<?xml version="1.0"?>
<Articles JournalTitle="Iranian Journal of Allergy, Asthma and Immunology">
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>19</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2020</Year>
        <Month>08</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Rhinitis as the Presenting Symptom of Pineal Region Epidermoid Tumor:  A Case Report</title>
    <FirstPage>452</FirstPage>
    <LastPage>455</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Joudi</LastName>
        <affiliation locale="en_US">Department of Immunology and Allergy, Allergy Research Center, Mashhad University  of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hosein</FirstName>
        <LastName>Eshaghi Ghalibaf</LastName>
        <affiliation locale="en_US">Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Atefeh</FirstName>
        <LastName>Ghorbanzadeh</LastName>
        <affiliation locale="en_US">Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Samira</FirstName>
        <LastName>Zabihyan</LastName>
        <affiliation locale="en_US">Department of Neurosurgery, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nasrin</FirstName>
        <LastName>Moazzen</LastName>
        <affiliation locale="en_US">Department of Pediatric Immunology and Allergy, Akbar Medical Center, Mashhad University  of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Khoshkhui</LastName>
        <affiliation locale="en_US">Department of Immunology and Allergy, Allergy Research Center, Mashhad University  of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>12</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>03</Month>
        <Day>10</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Brain tumors are the rarest cause of cerebrospinal fluid rhinorrhea. Non-traumatic cerebrospinal fluid&#xA0;rhinorrhea&#xA0;is also a relatively rare condition. It may be misdiagnosed as allergic rhinitis or chronic sinusitis and lead to unsuitable treatment. We described a 34-year-old man who came to our allergy clinic with a chief complaint of clear rhinorrhea from his left nostril with more than four years of duration. Onlyhypertrophy of left inferior concha was found in the clinical examination. His rhinorrhea aggravated when bending forward. So we were suspicious of CSF rhinorrhea. MRI was done for him and demonstrated a large tumor in the pineal region. The patient underwent surgery with resection of the mass via an infratentorial-supracerebellar approach. This case showed the role of maintaining differential diagnosis for a common complaint; rhinitis which is seen as usual.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2308</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>19</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2020</Year>
        <Month>08</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Intravenous Immunoglobulin Therapy in Myocarditis</title>
    <FirstPage>323</FirstPage>
    <LastPage>336</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Amir Hossein</FirstName>
        <LastName>Mansourabadi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ladan</FirstName>
        <LastName>Gol Mohammad pour Afrakoti</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abbas</FirstName>
        <LastName>Shabanian</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Students Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Reza</FirstName>
        <LastName>Shabanian</LastName>
        <affiliation locale="en_US">3 Department of Pediatric Cardiology, Children&#x2019;s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Aliakbar</FirstName>
        <LastName>Amirzargar</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>09</Month>
        <Day>14</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>04</Month>
        <Day>02</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Myocarditis is an inflammatory disease of the myocardium with lymphocyte infiltration and myocyte necrosis leading to a wide range of clinical presentations including heart failure, arrhythmia, and cardiogenic shock. Infectious and noninfectious agents may trigger the disease. The fact that immunosuppressive drugs are useful in several kinds of autoimmune myocarditis is proof of the autoimmune mechanisms involved in the development of myocarditis. Pathogenic mechanisms in myocardial inflammation are including inflammasome activation followed by myocyte destruction, myocarditis, and pericarditis. Intravenous immunoglobulin (IVIG) is a serum product made up of immunoglobulins, widely used in a variety of diseases. This product is effective in several immune-mediated pathologies. As well as the determined usage of IVIG in Kawasaki disease, IVIG may be useful in several kinds of heart failure including fulminant myocarditis, acute inflammatory cardiomyopathy, Giant Cell Myocarditis, and peripartum cardiomyopathy. Generally, IVIG is used in two different doses of low dose (200 to 400 mg/kg) and high dose (2 g/kg) regimen. The exact therapeutic effects of IVIG are not clear, however over the last decades, our knowledge about its mechanism of function has greatly enhanced. IVIG administration should be based on the accepted protocols of its transfusion. In this review article, we try to provide an overview of the different kinds of myocarditis, pathologic mechanisms and their common treatments and evaluation of the administration of IVIG in these diseases. Furthermore, we will review current protocols using IVIG in each disease individually.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2520</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>19</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2020</Year>
        <Month>08</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Fibroblast Growth Factor 2 Augments Transforming Growth Factor Beta 1 Induced Epithelial-mesenchymal Transition in Lung Cell Culture Model</title>
    <FirstPage>348</FirstPage>
    <LastPage>361</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Lamis</FirstName>
        <LastName>El-Baz</LastName>
        <affiliation locale="en_US">Department of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago,  Chicago, Illinois, USA AND Department of Zoology, Faculty of Science, Suez University, Suez, Egypt</affiliation>
      </Author>
      <Author>
        <FirstName>Nahla</FirstName>
        <LastName>Shoukry</LastName>
        <affiliation locale="en_US">Department of Zoology, Faculty of Science, Suez University, Suez, Egypt</affiliation>
      </Author>
      <Author>
        <FirstName>Hani</FirstName>
        <LastName>Hafez</LastName>
        <affiliation locale="en_US">Department of Zoology, Faculty of Science, Suez University, Suez, Egypt</affiliation>
      </Author>
      <Author>
        <FirstName>Robert</FirstName>
        <LastName>Guzy</LastName>
        <affiliation locale="en_US">Department of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago,  Chicago, Illinois, USA</affiliation>
      </Author>
      <Author>
        <FirstName>Mohamed</FirstName>
        <LastName>Salem</LastName>
        <affiliation locale="en_US">Department of Immunology and Biotechnology, Faculty of Science, Center of Excellence in  Cancer Research, Tanta University, Tanta, Egypt</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2020</Year>
        <Month>02</Month>
        <Day>15</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>05</Month>
        <Day>27</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Impaired lung epithelial cell regeneration following injury may contribute to the development of pulmonary fibrosis. Epithelial-mesenchymal transition (EMT) is a critical event in embryonic development, wound healing following injury, and even cancer progression. Previous studies have shown that the combination of transforming growth factor beta-1 (TGF&#x3B2;1) and fibroblast growth factor 2 (FGF2) induces EMT during cancer metastasis. However, this synergy remains to be elucidated in inducing EMT associated with wound healing after injury. We set out this study to determine the effect of fibroblast growth factor 2 (FGF2) on TGF&#x3B2;1-induced EMT in the human lung epithelium.
BEAS-2B and A549 cells were treated with TGF&#x3B2;1, FGF2, or both. EMT phenotype was investigated morphologically and by measuring mRNA expression levels; using quantitative real-time PCR. E-cadherin expression was assayed by western blot and immunofluorescence staining. Cell migration was confirmed using a wound-healing assay.
TGF&#x3B2;1 induced a morphological change and a significant increase in cell migration of BEAS-2B cells. TGF&#x3B2;1 significantly reduced E-cadherin (CDH1) mRNA expression and markedly induced expression of N-cadherin (CDH2), tenascin C (TNC), fibronectin (FN), actin alpha 2 (ACTA2), and collagen I (COL1A1). While FGF2 alone did not significantly alter EMT gene expression, it enhanced TGF&#x3B2;1-induced suppression of CDH1 and upregulation of ACTA2, but not TNC, FN, and CDH2. FGF2 significantly inhibited TGF&#x3B2;1-induced COL1A1 expression. Furthermore, FGF2 maintained TGF&#x3B2;1-induced morphologic changes and increased the migration of TGF&#x3B2;1-treated cells.
This study suggests a synergistic effect between TGF&#x3B2;1 and FGF2 in inducing EMT in lung epithelial cells, which may play an important role in wound healing and tissue repair after injury.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2712</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>19</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2020</Year>
        <Month>08</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Aspirin Sensitivity in Patients with Moderate to Severe Asthma</title>
    <FirstPage>447</FirstPage>
    <LastPage>451</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Saba</FirstName>
        <LastName>Arshi</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Narges</FirstName>
        <LastName>Eslami</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Mofid Hospital, Shahid Beheshti  University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Nabavi</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Bemanian</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Morteza</FirstName>
        <LastName>Fallahpour</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sima</FirstName>
        <LastName>Shokri</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Javad</FirstName>
        <LastName>Ahmadian</LastName>
        <affiliation locale="en_US">Department of Pediatric, Emam Reza Hospital, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Rasool</FirstName>
        <LastName>Molatefi</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Bu Ali Hospital, Ardebil University of Medical Sciences, Ardebil, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Kyan</FirstName>
        <LastName>Darabi</LastName>
        <affiliation locale="en_US">Iran Allergy Clinics, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Golam Reza</FirstName>
        <LastName>Sedighi</LastName>
        <affiliation locale="en_US">Department of Pediatric, Afzalipour Hospital, Kerman University of Medical Sciences, Kerman, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zeinab</FirstName>
        <LastName>Moinfar</LastName>
        <affiliation locale="en_US">Department of Community Medicine, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sepideh</FirstName>
        <LastName>Darougar</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2020</Year>
        <Month>03</Month>
        <Day>10</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>06</Month>
        <Day>22</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Asthma induced by ingestion of aspirin occurs when symptoms arise within 30 minutes to three hours after aspirin consumption. Previous data indicate that sensitivity to aspirin may be associated with poorly controlled asthma. This study aims to evaluate the frequency of aspirin sensitivity in patients with moderate to severe asthma receiving conventional asthma therapy.
This clinical trial was conducted on 65 patients aged 18 to 65 years with moderate to severe asthma from February 2015 to February 2016 at the Allergy Department, Hazrat-e-Rasoul Hospital, Iran University of Medical Sciences, Tehran. To assess treatment responses in patients, forced expiratory volume in the first second (FEV1) and asthma control test (ACT) scores were measured&#xA0;at baseline and after 3 months.
The results of the oral aspirin challenge revealed a prevalence of 35.38% for sensitivity to aspirin. Hypersensitivity reactions to aspirin were detected in 60.9% of the patients with moderate asthma and 39.1% of the patients with severe asthma. All patients with positive aspirin challenge tests suffered from rhinosinusitis and in 56.5% of cases, history of previous hypersensitivity reactions to non-steroidal anti-inflammatory drugs (NSAIDs) was detected. No meaningful differences were found between those patients with aspirin sensitivity and those with aspirin tolerance neither in mean pre-bronchodilator FEV1 nor in ACT scores pre- and post-treatment.
To conclude, aspirin sensitivity was not found to have an association with an unfavorable response to conventional treatment in patients with uncontrolled asthma.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2741</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>19</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2020</Year>
        <Month>08</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Association between Two Single Nucleotide Polymorphisms of Thymic Stromal Lymphopoietin (TSLP) Gene and Asthma in Iranian Population</title>
    <FirstPage>362</FirstPage>
    <LastPage>372</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Maral</FirstName>
        <LastName>Ranjbar</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mojdeh</FirstName>
        <LastName>Matloubi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad-Ali</FirstName>
        <LastName>Assarehzadegan</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Science, Tehran, Iran AND Immunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Morteza</FirstName>
        <LastName>Fallahpour</LastName>
        <affiliation locale="en_US">Department of Allergy, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran AND Firoozabadi Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Fatemeh</FirstName>
        <LastName>Sadeghi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Saeed</FirstName>
        <LastName>Soleyman-Jahi</LastName>
        <affiliation locale="en_US">Digestive Diseases Research Core Center, Division of Gastroenterology, School of Medicine, Washington University, St. Louis, USA</affiliation>
      </Author>
      <Author>
        <FirstName>Leila</FirstName>
        <LastName>Janani</LastName>
        <affiliation locale="en_US">Department of Biostatistics, School of Public Health, Iran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>12</Month>
        <Day>05</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>04</Month>
        <Day>11</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Thymic stromal lymphopoietin (TSLP) is a cytokine similar to IL-7, which is released by airway epithelial cells in response to injury and inflammation. Current literature is contradictory about the association between different single nucleotide polymorphisms (SNPs) of the TSLP gene and asthma development in different countries.
We aimed to evaluate the association between two common TSLP SNPs (rs2289276 and rs2289278) and the risk of asthma in the Iranian population. Genotyping of the TSLP gene was performed in 126 adult asthmatic patients and 300 controls; using the TaqMan genotyping assay. Moreover, total serum IgE level and eosinophil count were assessed.
The results indicated that the TT genotype of rs2289276 was inversely associated with the risk of asthma (p=0.002). A similar inverse association was detected in subgroups of atopic (p=0.001) and non-atopic (p=0.005) asthma. Moreover, the TT genotype of this SNP was more prevalent in severe and late-onset categories of asthma. In subgroup analysis, a significant sex-specific association between rs2290276 and asthma was observed in women (p=0.004). The prevalence of rs2289276 was extremely low, which made it infeasible to perform any further analysis.
Overall, our findings indicated that rs2290276 SNP of the TSLP gene has a protective phenotype against asthma development in the Iranian population.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2624</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>19</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2020</Year>
        <Month>08</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Unfulfilled Inflammatory Resolution: A Key Factor in the Pathogenesis of Psoriasis</title>
    <FirstPage>337</FirstPage>
    <LastPage>347</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Zohreh</FirstName>
        <LastName>Jadali</LastName>
        <affiliation locale="en_US">School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>07</Month>
        <Day>29</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>06</Month>
        <Day>22</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Recent literature has highlighted the importance of chronic inflammation in psoriasis pathogenesis. Non-resolving inflammation can trigger progressive tissue damage and inflammatory mediator release which in turn perpetuate the inflammatory cycle. Under normal conditions, inflammatory responses are tightly controlled through several mechanisms that restore normal tissue function and structure. Defects in regulatory mechanisms of the inflammatory response can result in persistent unresolved inflammation and further increases of inflammation. Therefore, this review focuses on defects in regulatory mechanisms of inflammatory responses that lead to uncontrolled chronic inflammation in psoriasis. Databases such as Pubmed Embase, ISI, and Iranian databases including Iranmedex, and SID were researched to identify relevant literature. The results of this review indicate that dysregulation of the inflammatory response may be a likely cause of various immune-mediated inflammatory disorders such as psorchool of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Ajami</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zahra</FirstName>
        <LastName>Mirsanei</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sima</FirstName>
        <LastName>Habibi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Bahador</FirstName>
        <LastName>Makkiabadi</LastName>
        <affiliation locale="en_US">Department of Medical Physics and Biomedical Engineering, School of Medicine, Tehran University  of Medical Sciences, Tehran, Iran AND Research Center for Biomedical Technologies and Robotics (RCBTR), Tehran University  of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Jamshid</FirstName>
        <LastName>Hadjati</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Amir</FirstName>
        <LastName>Jafari</LastName>
        <affiliation locale="en_US">Department of Medical Physics and Biomedical Engineering, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Research Center for Biomedical Technologies and Robotics (RCBTR), Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2021</Year>
        <Month>08</Month>
        <Day>30</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2021</Year>
        <Month>09</Month>
        <Day>13</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">This study is designed to present an agent-based model (ABM) to simulate the interactions between tumor cells and the immune system in the melanoma model. The Myeloid-derived Suppressor Cells (MDSCs) and dendritic cells (DCs) are considered in this model as immunosuppressive and antigen-presenting agents respectively.
The animal experiment was performed on 68 B16F10 melanoma tumor-bearing C57BL/6 female mice to collect dynamic data for ABM implementation and validation. Animals were divided into 4 groups; group 1 was control (no treatment) while groups 2 and 3 were treated with DC vaccine and low-dose 5- fluorouracil (5-FU) respectively and group 4 was treated with both DC Vaccine and low-dose of 5-FU. The tumor growth rate, number of MDSC, and presence of CD8+/CD107a+ T cells in the tumor microenvironment were evaluated in each group. Firstly,&#xA0;the tumor cells, the effector immune cells, DCs, and the MDSCs have been considered as the agents of the ABM model and their interaction methods have been extracted from the literature&#xA0;and implemented in the model. Then, the model parameters were estimated by the dynamic data collected from animal experiments.&#xA0;
To validate the ABM model, the simulation results were compared with the real data. The results show that the dynamics of the model agents can mimic the relations among considered immune system components to an emergent outcome compatible with real data. The simplicity of the proposed model can help to understand the results of the combinational therapy and make this model a useful tool for studying different scenarios and assessing the combinational results. 
Determining the role of each component helps to find critical times during tumor progression and change the tumor and immune system balance in favor of the immune system.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3343</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3343/1827</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>21</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>04</Month>
        <Day>11</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Decrease of Tumor-infiltrating Regulatory T Cells Using Pentoxifylline:  An Ex Vivo Analysis in Triple-negative Breast Cancer Mouse Model</title>
    <FirstPage>167</FirstPage>
    <LastPage>177</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Mohammad Hossein</FirstName>
        <LastName>Kazemi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran AND Department of ATMP, Breast Cancer Research Center, Motamed Cancer Institute,  ACECR, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahdieh</FirstName>
        <LastName>Shokrollahi Barough</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran AND Department of ATMP, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Alireza</FirstName>
        <LastName>Ghanavatinejad</LastName>
        <affiliation locale="en_US">Department of Immunology, Pasteur Institute of Iran, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zahra</FirstName>
        <LastName>Momeni-Varposhti</LastName>
        <affiliation locale="en_US">Hematopoietic Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Samaneh</FirstName>
        <LastName>Khorrami</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran AND Immunology Research Center, Institute of Immunology and Infectious Disease, Iran University  of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Behnam</FirstName>
        <LastName>Sadeghi</LastName>
        <affiliation locale="en_US">Department of ATMP, Breast Cancer Research Center, Motamed Cancer Institute,  ACECR, Tehran, Iran AND Division of Pediatrics, Department of Clinical Science, Translational Cell Therapy Research (TCR), Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm, Sweden</affiliation>
      </Author>
      <Author>
        <FirstName>Reza</FirstName>
        <LastName>Falak</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran AND Immunology Research Center, Institute of Immunology and Infectious Disease, Iran University  of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2021</Year>
        <Month>08</Month>
        <Day>17</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2021</Year>
        <Month>11</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Triple-negative breast cancer (TNBC) is the most aggressive type of BC with the highest percentage of tumor-infiltrating lymphocytes (TILs). Hence, TIL therapy is considered a promising approach to target TNBC. Depletion of regulatory T cells (Tregs) in TILs can improve the antitumor function of TIL therapy. Pentoxifylline (PTXF) is a xanthine derivative that can modulate the nuclear factor kappa B (NF-&#x3BA;B) signaling and probably affect the Treg proportion in TILs. We aimed to evaluate the ex vivo effect of PTXF on the proportion of Treg cells in the TILs derived from a mouse model of TNBC.
The 4T1 cells were inoculated subcutaneously to BALB/c mice to induce TNBC. TILs were isolated from tumor tissue by enzymatic digestion and cultured alone or with 4T1 cells for 24, 48, and 72 h in the presence of interleukin (IL)-2 and different concentrations of PTXF. The toxicity of PTXF and its effects on Tregs proportion as well as cytokine production was evaluated using MTT assay, flow cytometry, and ELISA, respectively.
PTXF had no significant impact on the viability of TILs. Both 500 and 1000 mg/mL of PTXF decreased the proportion of Tregs in a dose-dependent manner. The level of interferon-g and tumor growth factor-b in TILs supernatant was increased and decreased, respectively.
Our data suggest that ex vivo treatment of TILs with pentoxifylline could decrease the proportion of Tregs in the conventional IL-2-mediated TIL expansion and change the cytokine balance of TILs in favor of antitumor immune response.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3326</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3326/1828</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>21</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>04</Month>
        <Day>11</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Effects of PI3K/Akt/mTOR Signaling Pathway Inhibitors on the Expression of Immune Checkpoint Ligands in Acute Myeloid Leukemia Cell Line</title>
    <FirstPage>178</FirstPage>
    <LastPage>188</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Saeid</FirstName>
        <LastName>Taghiloo</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran AND Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Saeid</FirstName>
        <LastName>Norozi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hossein</FirstName>
        <LastName>Asgarian-Omran</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran AND Gastrointestinal Cancer Research Center, Non-Communicable Diseases Institute, Mazandaran University  of Medical Sciences, Sari, Iran AND Immunogenetics Research Center, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2021</Year>
        <Month>07</Month>
        <Day>03</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>02</Month>
        <Day>11</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Up-regulation of immune checkpoint ligands is considered as one of the most important immune escape mechanisms in acute myeloid leukemia (AML). Herein, we investigate a relationship between the inhibition of PI3K/Akt/mTOR signaling pathways and the regulation of immune checkpoint ligands in AML cells.
The HL-60 cell line was treated with idelalisib as PI3K inhibitor, MK-2206 as Akt inhibitor, and everolimus as mTOR inhibitor either in a single or combined format. Cell viability and apoptosis were evaluated using MTT and flow cytometry assays, respectively. The relative expression of PD-L1, galectin-9, and CD155 was determined by real-time PCR.
Our findings demonstrated decreased proliferation and increased apoptosis of HL-60 cells after treatment with idelalisib, MK-2206, and everolimus. As expected, the combined treatment showed a more inhibiting effect than the single treatment. Interestingly, our results elucidated that the expression of PD-L1 and Gal-9 but not MK-2206 decreased after treatment with idelalisib and everolimus. Regarding CD155, the expression of this molecule was downregulated after treatment with everolimus, but not idelalisib and MK-2206. However, combined treatment of HL-60 cells with two or three inhibitors decreased the expression levels of PD-L1, Gal-9, and CD155 checkpoint ligands.
We showed that PI3K/Akt/mTOR pathway inhibitors not only serve as cytotoxic drugs but also regulate the expression of immune checkpoint ligands and interfere with the immune evasion mechanisms of AML leukemic cells. Combinational treatment approaches to block these pathways might be a promising and novel therapeutic strategy for AML patients via interfering in immune escape mechanisms.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3279</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3279/1829</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>21</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>04</Month>
        <Day>11</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Role of HLA-DRB1 Alleles in Pulmonary Cystic Fibrosis</title>
    <FirstPage>189</FirstPage>
    <LastPage>196</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Alireza</FirstName>
        <LastName>Asef</LastName>
        <affiliation locale="en_US">Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hossein Ali</FirstName>
        <LastName>Ghafaripour</LastName>
        <affiliation locale="en_US">Pediatric Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung  Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamidreza</FirstName>
        <LastName>Jamaati</LastName>
        <affiliation locale="en_US">Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Varahram</LastName>
        <affiliation locale="en_US">Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis  and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ian</FirstName>
        <LastName>M. Adcock</LastName>
        <affiliation locale="en_US">Cell and Molecular Biology Group, Airways Disease Section, National Heart and Lung Institute, Imperial College London, London, UK AND Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, The University of Newcastle, Newcastle, New South Wales, Australia</affiliation>
      </Author>
      <Author>
        <FirstName>Esmaeil</FirstName>
        <LastName>Mortaz</LastName>
        <affiliation locale="en_US">Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis  and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran AND Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2021</Year>
        <Month>03</Month>
        <Day>09</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2021</Year>
        <Month>10</Month>
        <Day>04</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Cystic fibrosis (CF) is the most common lethal autosomal recessive disease in white Caucasians. It affects many organs including the lung, pancreas, and liver. Whilst CF is a monogenic disease, several studies revealed a complex relationship between genotype and clinical phenotype of diseases. We examined the expression of human leukocyte antigen (HLA) class II alleles among Iranian CF patients with disease-related microbial infection.
This study was conducted on 50 hospitalized CF patients (27 males, 23 females aged 15.5&#xB1;6.5 years), and 50 healthy age- and gender-matched control subjects. 5ml whole blood was harvested and after isolation of genomic DNA, HLA-DRB1 subtypes were determined by single specific primer polymerase chain reaction methods.
HLA-DRB1*10 was less frequent and HLA-DRB1*04 and HLA-DRB1*11 was the most frequent allele in CF patients, but none reached significance. HLA-DRB1*04 allele was frequently seen among16 CF patients with high serum IgE levels (430.25&#xB1;219.7 IU/mL) and 27 CF patients that were positive for Pseudomonas aeruginosa colonization. A total of 31 CF patients had candida Albicans colonization in whom HLA-DRB1*11 was mostly seen. A total of 3 CF patients had allergic bronchopulmonary aspergillosis and two were diabetic.
The DR4 and DR11 serotypes that recognize the HLA-DRB1*04 and HLA-DRB1*11 gene products respectively are not significantly enriched in the Iranian CF population. Further research should be conducted on DR4 and DR11 in CF patients to understand their possible role in infection and IgE expression.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3145</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3145/1830</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>21</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>04</Month>
        <Day>11</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Clinical and Laboratory Parameters of Autoinflammatory Disorders in Single Tertiary Care Center</title>
    <FirstPage>197</FirstPage>
    <LastPage>206</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Roya</FirstName>
        <LastName>Sherkat</LastName>
        <affiliation locale="en_US">Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Alireza</FirstName>
        <LastName>Rafiei</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Vida</FirstName>
        <LastName>Homayouni</LastName>
        <affiliation locale="en_US">Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Elmira</FirstName>
        <LastName>Kalantari</LastName>
        <affiliation locale="en_US">Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Roya</FirstName>
        <LastName>Sepahvandi</LastName>
        <affiliation locale="en_US">Non-communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sahar</FirstName>
        <LastName>Memarmontazarin</LastName>
        <affiliation locale="en_US">Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ali</FirstName>
        <LastName>Mosayebian</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2021</Year>
        <Month>07</Month>
        <Day>17</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2021</Year>
        <Month>10</Month>
        <Day>10</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Autoinflammatory diseases (AIDs) are disorders with an inborn error of innate immunity, characterized by recurrent episodes of fever and inflammatory attacks. The spectrum of AIDs is expanding, but there are no standardized clinical criteria for the diagnosis of the patients. This study aims at establishing the first autoinflammatory registry of an Iranian population focusing on the clinical and laboratory features that may help clinicians for a better understanding and diagnosis of these disorders.
Clinical and laboratory characteristics of patients who were clinically and or genetically diagnosed with AIDs were collected during 15 years. The updated version of classification criteria from the Eurofever Registry was used for the clinical diagnosis.
Twenty-eight patients (16 males and 12 females) with the mean&#xB1;SD age of 28.03&#xB1;14.49 years (from 2 to 68 years) were entered this study. About 29% were genetically diagnosed. Familial Mediterranean fever (FMF) was the most common diagnosis of the patients. Fever duration episodes were between 1-10 days. Some of the clinical manifestations from the most to the least common were as follows: arthralgia and arthritis (80%), myalgia (76%), coughs and shortness of breath (68%), fatigue (60%), abdominal pain (56%), increased erythrocyte sedimentation rate(ESR) (48%), and splenomegaly (24%).
Here, we presented the most common clinical manifestations of Iranian AIDs who have registered in our AID registry which would be a useful guide for managing the same patients and also designing the future studies.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3294</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3294/1831</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>21</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>04</Month>
        <Day>11</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Modulation of Immune Responses Against HA1 Influenza Vaccine Candidate by B-lymphocyte Stimulator Cytokine in Mice</title>
    <FirstPage>207</FirstPage>
    <LastPage>214</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Seyedeh Mahsa</FirstName>
        <LastName>Bagheri Yazdi</LastName>
        <affiliation locale="en_US">Razi Vaccine and Serum Research Institute, Agricultural Research Education and Extension Organization, Karaj, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Shahla</FirstName>
        <LastName>Shahsavandi</LastName>
        <affiliation locale="en_US">Razi Vaccine and Serum Research Institute, Agricultural Research Education and Extension Organization, Karaj, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Fatemeh</FirstName>
        <LastName>Fotouhi</LastName>
        <affiliation locale="en_US">Department of Influenza, Pasteur Institute of Iran, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Majid</FirstName>
        <LastName>Tebianian</LastName>
        <affiliation locale="en_US">Razi Vaccine and Serum Research Institute, Agricultural Research Education and Extension Organization, Karaj, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Majid</FirstName>
        <LastName>Ebrahimi</LastName>
        <affiliation locale="en_US">Razi Vaccine and Serum Research Institute, Agricultural Research Education and Extension Organization, Karaj, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2021</Year>
        <Month>06</Month>
        <Day>28</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2021</Year>
        <Month>12</Month>
        <Day>05</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Utilizing subunit vaccines is one of the strategies to address influenza infection. Recent innovations have focused on high doses of vaccine antigens and immune enhancers or adjuvant to induce more robust and long-lasting immune responses. Here, an effect of the B cell-activating factor receptor (BAFF-R) to increase the magnitude and durability of immune responses of the recombinant HA1 (rHA1) protein against the H1N1 influenza virus was studied.
The HA1 protein and the effector domain of BAFF-R were expressed in the pET-28a (+) vector. Eight-week-old BALB/c mice were equally grouped into five groups (n=20). The 15 and 25 &#x3BC;g/&#x3BC;L of rHA1 were mixed with 2 &#x3BC;g/&#x3BC;L of rBAFF-R and injected three times for vaccinated groups. Three control groups were received normal saline and two concentrations of rHA1. The ability of rBAFF-R in eliciting HA-specific antibody response and stimulating T lymphocyte proliferation to induce the cell-mediated immunity was assayed. Induction of protection was evaluated following the challenge with PR8 strain.
Analysis of immune responses showed that the co-administration of rBAFF-R with rHA1 boosted HI responses to the antigen in mice, whilst it was not able to promote the T cell proliferation responses against influenza. Compared to rHA1alone, the rBAFF-R/rHA1 generated efficient protection for the animals. There were no significant differences in eliciting the immune responses in mice immunized with the lower dose of rHA1 than that with the higher dose.
The data indicate the rBAFF-R can enhance the primary and memory immune responses to protect against influenza infection.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3277</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3277/1832</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>21</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>04</Month>
        <Day>11</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Korean Adolescent Patient with Manifestations of Lymphocyte Variant Hypereosinophilic Syndrome and Episodic Angioedema with Eosinophilia, Treated with Reslizumab</title>
    <FirstPage>215</FirstPage>
    <LastPage>218</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Jie Hee</FirstName>
        <LastName>Jue</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Keimyung University School of Medicine, Keimyung University Dongsan Hospital, Daegu, Korea</affiliation>
      </Author>
      <Author>
        <FirstName>Ye Jee</FirstName>
        <LastName>Shim</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Keimyung University School of Medicine, Keimyung University Dongsan Hospital, Daegu, Korea</affiliation>
      </Author>
      <Author>
        <FirstName>Sunggyun</FirstName>
        <LastName>Park</LastName>
        <affiliation locale="en_US">Department of Laboratory Medicine, Keimyung University School of Medicine, Keimyung University Dongsan Hospital, Daegu, Korea</affiliation>
      </Author>
      <Author>
        <FirstName>Do-Hoon</FirstName>
        <LastName>Kim</LastName>
        <affiliation locale="en_US">Department of Laboratory Medicine, Keimyung University School of Medicine, Keimyung University Dongsan Hospital, Daegu, Korea</affiliation>
      </Author>
      <Author>
        <FirstName>Hye Ra</FirstName>
        <LastName>Jung</LastName>
        <affiliation locale="en_US">Department of Pathology, Keimyung University School of Medicine, Keimyung Univ