<?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>21</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>12</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Identification of New Potential Allergens from Green-lipped Mussel  (Perna Canaliculus)</title>
    <FirstPage>711</FirstPage>
    <LastPage>715</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Paula</FirstName>
        <LastName>Kage</LastName>
        <affiliation locale="en_US">Department of Dermatology, Venereology and Allergology, UMC Leipzig, Leipzig, Germany</affiliation>
      </Author>
      <Author>
        <FirstName>Kristin</FirstName>
        <LastName>Schubert</LastName>
        <affiliation locale="en_US">Department of Molecular Systems Biology, Helmholtz-Centre for Environmental Research, Leipzig, Germany</affiliation>
      </Author>
      <Author>
        <FirstName>Regina</FirstName>
        <LastName>Treudler</LastName>
        <affiliation locale="en_US">Department of Dermatology, Venereology and Allergology, UMC Leipzig, Leipzig, Germany</affiliation>
      </Author>
      <Author>
        <FirstName>Jan-Christoph</FirstName>
        <LastName>Simon</LastName>
        <affiliation locale="en_US">Department of Dermatology, Venereology and Allergology, UMC Leipzig, Leipzig, Germany</affiliation>
      </Author>
      <Author>
        <FirstName>Martin</FirstName>
        <LastName>von Bergen</LastName>
        <affiliation locale="en_US">Department of Molecular Systems Biology, Helmholtz-Centre for Environmental Research, Leipzig, Germany AND Institute of Biochemistry, Faculty of Life Sciences, University of Leipzig, Leipzig, Germany</affiliation>
      </Author>
      <Author>
        <FirstName>Janina</FirstName>
        <LastName>Tomm</LastName>
        <affiliation locale="en_US">Department of Dermatology, Venereology and Allergology, UMC Leipzig, Leipzig, Germany</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2021</Year>
        <Month>10</Month>
        <Day>12</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>08</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">The green-lipped mussel (Perna canaliculus) originates from New Zealand. To preserve the health benefits of green-lipped mussel meat, it is freeze-dried to make a long-lasting powder. The powder is used to treat arthritis because of its potential anti-inflammatory properties. The report describes a 54-year-old woman who developed immediate rhinoconjunctival and respiratory symptoms after inhaling green-lipped mussel powder she gave to her dog for arthritis.
A skin prick test with green-lipped mussel powder was performed. Protein extracts from P canaliculus were separated by sodium dodecyl&#x2013;sulfate polyacrylamide (SDS) gel electrophoresis and probed with serum from patients and serum preincubated with green-lipped mussel extract. Bound immunoglobulin E (IgE) was detected by specific anti-human-IgE antibodies, and IgE-binding proteins were subsequently identified by liquid chromatography and mass spectrometry.
The skin prick test was positive for green-lipped mussel. Specific IgE against green-lipped mussel extract was detected using Western immunoblotting. These potential allergenic proteins were identified by mass spectrometry as actin, tropomyosin, and paramyosin.
All three allergens are reported for the first time for P canaliculus. Actin is a major allergen in&#xA0;Paphia textile, paramyosin in Sarcoptes scarbiei, and tropomyosin in Haliotis discus. For all IgE-binding proteins, the software AllCatPro predicted high allergenicity, supporting our conclusion that these proteins from P canaliculus may also be allergenic. The identification of allergens from P canaliculus provides the opportunity for specific tests to assess the frequency of allergic reactions to P canaliculus.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3378</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3378/1890</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>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>12</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Detection of Novel Autoantibodies to Nucleolin's RNA-binding Domains as a Serum Tumor Biomarker Through ELISA</title>
    <FirstPage>616</FirstPage>
    <LastPage>625</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Fatemeh</FirstName>
        <LastName>Ezzatifar</LastName>
        <affiliation locale="en_US">Molecular and Cell biology Research Center, Faculty of Medicine, Mazandaran University  of Medical Sciences, Sari, Iran AND 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>Alireza</FirstName>
        <LastName>Rafiei</LastName>
        <affiliation locale="en_US">Molecular and Cell biology Research Center, Faculty of Medicine, Mazandaran University  of Medical Sciences, Sari, Iran AND Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Reza</FirstName>
        <LastName>Valadan</LastName>
        <affiliation locale="en_US">Molecular and Cell biology Research Center, Faculty of Medicine, Mazandaran University  of Medical Sciences, Sari, Iran AND 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</affiliation>
      </Author>
      <Author>
        <FirstName>Mahmood</FirstName>
        <LastName>Jeddi-Tehrani</LastName>
        <affiliation locale="en_US">Monoclonal Antibody Research Center, Avicenna Research Institute, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>08</Month>
        <Day>20</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Expression and location of nucleolin are often abnormal in malignancies, which may result in the production of autoantibodies. Despite this, the identification of such autoantibodies may be essential for the early diagnosis and prognosis of cancers.
In this investigation, the recombinant nucleolin protein was generated using an Escherichia coli expression system and was used an indirect enzyme-linked immunosorbent assay to detect anti-nucleolin autoantibodies in cancer patients' sera.
Lung cancer patients' autoantibodies displayed the highest seroreactivity with the recombinant protein, with area under the curve of 0.948 and sensitivity and specificity of 85% and 96.67%, respectively (accuracy=92%). Anti-nucleolin autoantibodies were linked with lung tumor size (r=0.793), tumor, node, metastasis staging (r=0.643), and proliferation (r=0.744).
These autoantibodies distinguished patients with early-stage lung cancer from healthy controls. Since anti-nucleolin autoantibodies are strongly linked to tumor size, clinical staging, and growth, they can be used to measure how well a treatment is working.&#xA0;&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3636</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3636/1892</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>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>12</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Comment on &#x201C;Effect of Loaded Glycyrrhizic Acid on PLGA Nano-particle  on Treatment of Allergic Asthma&#x201D;</title>
    <FirstPage>716</FirstPage>
    <LastPage>717</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Zahra</FirstName>
        <LastName>Asadi</LastName>
        <affiliation locale="en_US">Students Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran AND Department of Clinical Biochemistry, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Asad</FirstName>
        <LastName>Vaisi-Raygani</LastName>
        <affiliation locale="en_US">Department of Clinical Biochemistry, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Faranak</FirstName>
        <LastName>Aghaz</LastName>
        <affiliation locale="en_US">Nano Drug Delivery Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>06</Month>
        <Day>05</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>10</Month>
        <Day>10</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">No Abstract&#xA0;No Abstract&#xA0;No AbstractNo Abstract</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3564</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3564/1905</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>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>12</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Soluble and Immobilized Anti-CD3/28 Distinctively Expand and Differentiate Primary Human T Cells: An Implication for Adoptive T Cell Therapy</title>
    <FirstPage>630</FirstPage>
    <LastPage>637</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Tahereh</FirstName>
        <LastName>Soltantoye</LastName>
        <affiliation locale="en_US">Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Behnia</FirstName>
        <LastName>Akbari</LastName>
        <affiliation locale="en_US">Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamid Reza</FirstName>
        <LastName>Mirzaei</LastName>
        <affiliation locale="en_US">Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Jamshid</FirstName>
        <LastName>Hadjati</LastName>
        <affiliation locale="en_US">Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>07</Month>
        <Day>26</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>10</Month>
        <Day>24</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Cell-based cancer therapies have led to a paradigm shift in the treatment of patients with various cancers. To date, a vast majority of cancer immunotherapies have used genetically engineered T cells to target tumors. Stimulation and ex vivo expansion of T cells, as one of the crucial starting materials for T cell manufacturing, have always been a critical part of adoptive T-cell therapy (ACT). Typically, anti-CD3 and anti-CD28 monoclonal antibodies (mAbs) along with interleukin-2 (IL-2), through transducing signals one, two, and three, respectively, are essential for in vitro T cell activation. Terminal differentiation and replicative senescence are the main barriers of the ACTs during the manufacturing of engineered T cells ex vivo.In 
this study, we aimed to compare the T cell activation protocol that we&#xA0; developed in our lab (soluble anti-CD3/28 mAbs) with a common T cell activation protocol (immobilized anti-CD3/soluble anti-CD28) in terms of T cell expansion, activation, immunophenotype, and cellular fate.
We observed that T cells were equally expanded in both protocols. Notably, our modified protocol promoted the outgrowth of CD8+ T cells postactivation. Concerning the low concentrations of both soluble anti-CD3 and anti-CD28, the modified protocol could significantly enrich memory T cell subsets.
In conclusion, our data demonstrated that the soluble CD3/28 mAbs protocol is cost-effective and more efficient for generating more potent T cells, thereby expecting a better therapeutic outcome.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3613</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3613/1891</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>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>12</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Importance of STAT3 Polymorphisms on the Risk and Clinical Characteristics of Rheumatoid Arthritis</title>
    <FirstPage>638</FirstPage>
    <LastPage>645</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Amirhossein</FirstName>
        <LastName>Salehi</LastName>
        <affiliation locale="en_US">Division of Rheumatology, Department of Internal Medicine, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ebrahim</FirstName>
        <LastName>Hazrati</LastName>
        <affiliation locale="en_US">Department of Anesthesiology and Intensive Care, Medical Faculty, AJA University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamta</FirstName>
        <LastName>Ranjbar</LastName>
        <affiliation locale="en_US">Student Research Committee, Kerman University of Medical Sciences, Kerman, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Javad</FirstName>
        <LastName>Behroozi</LastName>
        <affiliation locale="en_US">Department of Genetics and Advanced Medical Technology, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Bahram</FirstName>
        <LastName>Pakzad</LastName>
        <affiliation locale="en_US">Division of Rheumatology, Department of Internal Medicine, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Mousavi</LastName>
        <affiliation locale="en_US">Division of Rheumatology, Department of Internal Medicine, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mojtaba</FirstName>
        <LastName>Mousavi</LastName>
        <affiliation locale="en_US">Department of Internal Medicine, School of Medicine, Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Marzieh</FirstName>
        <LastName>Hossein Balam</LastName>
        <affiliation locale="en_US">Department of Internal Medicine, School of Medicine, Isfahan University of Medical Science, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mansour</FirstName>
        <LastName>Salesi</LastName>
        <affiliation locale="en_US">Department of Internal Medicine, School of Medicine, Isfahan University of Medical Science, Isfahan, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>10</Month>
        <Day>22</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>11</Month>
        <Day>29</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Signal transducer and activator of transcription 3 (STAT3) has been introduced as one of the critical genetic factors in the pathogenesis of rheumatoid arthritis (RA). Single nucleotide polymorphisms (SNPs) in microRNA binding sites, known as miRSNPs, are a class of common variants in the 3&#x2032; untranslated regions of genes targeted by miRNAs. miRSNPs unbalance gene expression by disrupting the binding regions of microRNAs. In this study, we intended to evaluate the association of two miRSNPs with the risk of RA development and its clinical features.
We studied 120 Iranian patients with RA and 125 non-RA subjects as controls. The genotypes and alleles of rs1053005 and rs1053023 in each individual were assessed by the high-resolution melting method.
The distribution of STAT3 variants did not differ markedly in RA patients compared to healthy controls. Stratification analysis revealed that rs1053005 was linked with a higher concentration of C-reactive protein and an increased erythrocyte sedimentation rate, two indicators of inflammation and disease activity in RA patients. The rs1053023 variant was correlated with higher levels of creatinine as an indicator of renal involvement.
Our data demonstrate an association between STAT3 variants and clinical characteristics of RA, such as disease activity and probably kidney impairment. &#xA0;However, we did not observe a significant relationship between the two targeted variants and a predisposition to RA.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/3682</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/3682/1906</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>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2022</Year>
        <Month>12</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">MicroRNAs Targeting Programmed Cell Death Protein 1 (PD-1) Promote Natural Killer Cell Exhaustion in Rheumatoid Arthritis</title>
    <FirstPage>646</FirstPage>
    <LastPage>656</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Hemmatzadeh</LastName>
        <affiliation locale="en_US">Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran AND Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran AND Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Elham</FirstName>
        <LastName>Ahangar Parvin</LastName>
        <affiliation locale="en_US">Department of Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Alireza</FirstName>
        <LastName>Ghanavatinejad</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Narges</FirstName>
        <LastName>Rostami</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehrzad</FirstName>
        <LastName>Hajaliloo</LastName>
        <affiliation locale="en_US">Connective Tissue Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Navid</FirstName>
        <LastName>Shomali</LastName>
        <affiliation locale="en_US">Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran AND Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran AND Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamed</FirstName>
        <LastName>Mohammadi</LastName>
        <affiliation locale="en_US">Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran AND Department of Immunology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Farhad</FirstName>
        <LastName>Jadidi-Niaragh</LastName>
        <affiliation locale="en_US">Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran AND Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>08</Month>
        <Day>15</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>10</Month>
        <Day>08</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">&#xA0;Natural killer (NK) cells play a role in the pathogenesis of rheumatoid arthritis (RA). Upregulated levels of programmed cell death protein 1 (PD-1) is a sign of exhausted NK cells that could be regulated by microRNAs (miRNAs). In this investigation, we determined PD&#x2011;1 expression on NK cells (as a representation of NK cell exhaustion) in RA patients and evaluated if miRNAs are involved in the modulation of PD-1 expression in NK cells.
Peripheral blood specimens were obtained from 40 RA patients and 20 healthy subjects. NK cells were isolated by negative selection from a pool of peripheral blood mononuclear cells. The frequency of PD-1&#x2013;expressing NK cells and the expression of PD-1 on NK cells were analyzed by flow cytometry. Real-time PCR was used to measure the expression levels of PD-1 mRNA and miRNAs in the NK cells.
The percentage of the PD-1&#x2013;expressing NK cells and Mean fluorescence intensity (MFI) of PD-1 expression on the NK cells were significantly higher in the RA cases compared to the controls. The mRNA expression of PD-1 was significantly upregulated in NK cells from RA patients compared to healthy subjects. The expression levels of miR-28, miR-138, and miR-4717 were significantly downregulated in the NK cells from RA patients compared to the healthy group.
In RA, miRNAs probably regulate the NK cell exhaustion process through driving PD-1 expression.</abstract>
    <web_url>https://ijaiasis. Based on current findings, advances in understanding the cellular and molecular mechanisms involved in inflammation resolution are not only improving our knowledge of the pathogenesis of chronic inflammatory diseases but also supporting the development of new therapeutic&#xA0;strategies.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2473</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">Enhancement of Anti-allergic Effect of Diethylcarbamazine Citrate in Asthmatic Mouse Model: Testing of Anti-drug Antibodies and Quercetin</title>
    <FirstPage>373</FirstPage>
    <LastPage>385</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Nosibah</FirstName>
        <LastName>Abdul-Razek</LastName>
        <affiliation locale="en_US">Department of Zoology, Immunity Division, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt</affiliation>
      </Author>
      <Author>
        <FirstName>Al-Mahy</FirstName>
        <LastName>M. El-Mallah</LastName>
        <affiliation locale="en_US">Department of Zoology, Immunity Division, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt</affiliation>
      </Author>
      <Author>
        <FirstName>Abdelaziz</FirstName>
        <LastName>Abuelsaad</LastName>
        <affiliation locale="en_US">Department of Zoology, Immunity Division, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt</affiliation>
      </Author>
      <Author>
        <FirstName>Mahmoud</FirstName>
        <LastName>Abdel-Latif</LastName>
        <affiliation locale="en_US">Department of Zoology, Immunity Division, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>12</Month>
        <Day>26</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>06</Month>
        <Day>11</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Diethylcarbamazine citrate (DEC) is known as an effective treatment for bronchial asthma because of its ability to reduce eosinophil trafficking to the lung tissue. The current study aimed to potentiate the anti-allergic effect of the drug by passive immunization of the asthmatic model with anti-DEC antibody or prior treatment with quercetin (Qur).
Eight mice groups were categorized into control, the model of lung asthma, treated with DEC, passively immunized with anti(&#x3B1;)-bovine serum albumin Ab, anti-DEC Ab, prior exposure to 10, 20, or 40 mg Qur/Kg. b.wt. Both eosinophil peroxidase (EPO) and eotaxin2 in the lung tissues were performed. Serum levels of cytokines, bronchoalveolar lavage fluid&#xA0; (BALF) IgE, rabbit anti-bovine serum albumin (anti-BSA), and DEC IgG in lung tissue homogenates were assayed by ELISA.
Regarding the effect of anti-DEC Ab and Qur on DEC-induced recovery of histopathological alterations showed that the Ova group had peri-bronchial hyperplasia, mononuclear leukocyte infiltration, thickening in the wall of alveoli, and congested blood vessels. However, the reduction of inflammatory cells and thickened alveolar walls was dependent on the Qur dose. Qur40 enhanced the anti-allergic effect of DEC. Moreover, the present data revealed high levels of Th2 cytokines (IL-4 and IL-5) and IgE in the Ova group. An increased leukocyte infiltration/thickening of the alveolar wall and lung tissue EPO/eotaxin2 were also observed. Qur-40 could show an enhancement effect on DEC for the reduction of IL-4, IL-5, IgE, EPO, and eotaxin 2. Consequently, the IFN-&#x3B3;/IL-4 ratio was increased.
Qur at 40 mg/Kg could be recommended to enhance the DEC effect suggesting a novel approach for treatment.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2654</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">The Relaxant Effect of Plantago Major on Rat Tracheal Smooth Muscles  and Its Possible Mechanisms</title>
    <FirstPage>386</FirstPage>
    <LastPage>396</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Javad</FirstName>
        <LastName>Boskabadi</LastName>
        <affiliation locale="en_US">Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran AND Department of Clinical Pharmacy, School of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Saeideh</FirstName>
        <LastName>Saadat</LastName>
        <affiliation locale="en_US">Department of Physiology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hosein</FirstName>
        <LastName>Boskabady</LastName>
        <affiliation locale="en_US">Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran AND Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>12</Month>
        <Day>06</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>03</Month>
        <Day>14</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">This study was conducted to evaluate the possible mechanisms of the relaxant effects of hydroalcoholic extract of Plantago major (P. major) on tracheal smooth muscle (TSM) in rats.
The effects of cumulative concentrations of P. major (5, 10, 20 and 40 mg/mL) and theophylline (0.2, 0.4, 0.6 and 0.8 mM) were evaluated on pre-contracted TSM with 10 &#x3BC;&#x39C; methacholine or 60 mM KCl. To determine the possible mechanisms, the relaxant effect of the plant was also examined on incubated TSM with atropine, indomethacin, chlorpheniramine, glibenclamide, diltiazem, papaverine, and propranolol.
The results indicated concentration-dependent relaxant effects for P. major in non-incubated TSM contracted by methacholine or KCl. There was no statistically significant difference in the relaxant effects of P. major between non-incubated and incubated tissues with indomethacin, papaverine, and propranolol. However, the relaxant effects of P. major in incubated tissues with atropine (p&lt;0.01 to p&lt;0.001), chlorpheniramine (p&lt;0.05 to p&lt;0.001), glibenclamide (p&lt;0.05), or diltiazem (p&lt;0.01) were significantly lower than non-incubated TSM.
P. major indicated relatively potent relaxant effects which were lower than those of theophylline. Muscarinic and histamine (H1) receptors inhibition, as well as calcium channel blocking and potassium channel opening effects are suggested to contribute to the TSM relaxant effect of the plant.
&#xD;

&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2626</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">Leucine-rich Repeats and Immunoglobulin 1 (LRIG1) Ameliorates Liver Fibrosis and Hepatic Stellate Cell Activation via Inhibiting Sphingosine Kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P) Pathway</title>
    <FirstPage>397</FirstPage>
    <LastPage>408</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Wei</FirstName>
        <LastName>Zhan</LastName>
        <affiliation locale="en_US">Department of Colorectal Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, China</affiliation>
      </Author>
      <Author>
        <FirstName>Xin</FirstName>
        <LastName>Liao</LastName>
        <affiliation locale="en_US">Department of Imaging, Affiliated Hospital of Guizhou Medical University, Guiyang, China</affiliation>
      </Author>
      <Author>
        <FirstName>Zhongsheng</FirstName>
        <LastName>Chen</LastName>
        <affiliation locale="en_US">Guizhou Medical University, Guiyang, China</affiliation>
      </Author>
      <Author>
        <FirstName>Lianghe</FirstName>
        <LastName>Li</LastName>
        <affiliation locale="en_US">Guizhou Medical University, Guiyang, China</affiliation>
      </Author>
      <Author>
        <FirstName>Tian</FirstName>
        <LastName>Tian</LastName>
        <affiliation locale="en_US">Guizhou Medical University, Guiyang, China AND  Department of Pathology, Guiyang Maternal and Child Health Hospital, Guiyang, China</affiliation>
      </Author>
      <Author>
        <FirstName>Rui</FirstName>
        <LastName>Li</LastName>
        <affiliation locale="en_US">Department of Traditional Chinese Medicine, Guizhou Provincial People&#x2019;s Hospital, Guiyang, China</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>06</Month>
        <Day>24</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>03</Month>
        <Day>10</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">To detect the leucine-rich repeats and immunoglobulin 1 (LRIG1) ameliorated liver fibrosis and hepatic stellate cell (HSC) activation via inhibiting sphingosine kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P) pathway.
C57BL/6 male mice (eight weeks old) were intraperitoneal injection with 10% carbon tetrachloride (CCl4) as an in vivo model. The LX-2 cells were induced as amodel for in vitro study by TGF-&#x3B2; (10 ng/mL).
The Hematoxylin-eosin (HE) staining, Masson staining, and Sirius red staining results showed that CCl4 caused serious fibrosis and injury in liver tissue, high expression of type I collagen &#x3B1;1 chain (Col1&#x3B1;1) and &#x3B1;-smooth muscle actin (&#x3B1;-SMA) in liver tissue, while the LRIG1 expression level was signi&#xFB01;cantly decreased in LX-2 cell lines. The LRIG1 ameliorated CCl4-induced liver fibrosis, indicated by the fibronectin, &#x3B1;-SMA, LRIG1, SphK1, Col1&#x3B1;1, fibrin Connexin 1 (Fn1), tissue inhibitor of metalloproteinase-1 (TIMP1), sphingosine-1-phosphate (S1P), transforming growth factor-beta 1 (TGF-&#x3B2;1) expression level changes. Similar results were observed in TGF-&#x3B2;1 treated of LX-2 cells. However, the effects were attenuated by treatment with LRIG1. Moreover, SphK1 inhibitors abrogated the effect of LRIG1 on fibrosis.
These results demonstrated that LRIG1 improved liver fibrosis in vitro and in vivo via suppressing the SphK1/S1P pathway, indicating its potential use in the treatment of liver fibrosis.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2443</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">Investigating the Relationship between Serum Levels of Interleukin-22 and Interleukin-1 Beta with Febrile Seizure</title>
    <FirstPage>409</FirstPage>
    <LastPage>415</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Ahmad</FirstName>
        <LastName>Talebian</LastName>
        <affiliation locale="en_US">Department of Pediatric Neurology, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Farzaneh</FirstName>
        <LastName>Hassani</LastName>
        <affiliation locale="en_US">Department of Pediatric Neurology, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hassan</FirstName>
        <LastName>Nikoueinejad</LastName>
        <affiliation locale="en_US">Nephrology and Urology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hossein</FirstName>
        <LastName>Akbari</LastName>
        <affiliation locale="en_US">Department of Biostatistics and Public Health, Faculty of Health, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2020</Year>
        <Month>03</Month>
        <Day>02</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>07</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">A febrile seizure is the most common type of seizure in young kids, which is not fully known. Inflammatory mediators can affect the pathogenesis of the disease. Considering the controversy about the impacts of interleukin 1 beta (IL-1&#x3B2;) and the lack of a study on interleukin 22 (IL-22), the purpose of the present study was to investigate the relationship between IL-22 and IL-1&#x3B2; serum levels with febrile seizure in young kids.
Our case-control study has been conducted on 120 young kids aged 6-60 months with the sign of the fever. Rectal temperature was measured for allcases. Patients with febrile seizure (n=60) and patients with fever and without a seizure (n=60) were investigated as case and control groups, respectively. Serum levels of IL-22 and IL-1&#x3B2; were measured in all participants through the ELISA method.
The serum level of IL-1&#x3B2; was significantly higher in the case group compared to the control group (p&#x2C2;0.001), while there were no significant differences between the two groups in terms of IL-22 (p=0.92). Unlike IL-1&#x3B2; (p&#x2264;0.021), IL-22 showed no difference between two groups according to some demographic and clinical features like gender, age group, family history of febrile seizure, family history of epilepsy, and evolutionary status (p&gt;0.22). Logistic multiple regression analysis showed that, unlike IL-1&#x3B2; (p&#x2C2;0.001), IL-22 does not change the chance of febrile seizure in the study groups (p=0.737).
The findings of this study indicated that, unlike IL-1&#x3B2;, IL-22 has not any changes/effects in the febrile seizure.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2734</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">Comparison of Expression Levels of miR-29b-3p and miR-326 in T Helper-1  and T Helper-17 Cells Isolated from Responsive and Non-responsive  Relapsing-remitting Multiple Sclerosis Patients Treated with Interferon-beta</title>
    <FirstPage>416</FirstPage>
    <LastPage>425</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Leila</FirstName>
        <LastName>Karimi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nahid</FirstName>
        <LastName>Eskandari</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Vahid</FirstName>
        <LastName>Shaygannejad</LastName>
        <affiliation locale="en_US">Isfahan Neurosciences Research Center, Alzahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nasrin</FirstName>
        <LastName>Zare</LastName>
        <affiliation locale="en_US">Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of  Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Alireza</FirstName>
        <LastName>Andalib</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hossein</FirstName>
        <LastName>Khanahmad</LastName>
        <affiliation locale="en_US">Department of Genetic and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Omid</FirstName>
        <LastName>Mirmosayyeb</LastName>
        <affiliation locale="en_US">Isfahan Neurosciences Research Center, Alzahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2020</Year>
        <Month>02</Month>
        <Day>04</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>08</Month>
        <Day>25</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">T helper type 1 (Th1) and Th17 Cells with distinct cytokine profiles including interferon-gamma (IFN-&#x3B3;) and interleukin 17 (IL-17) have a pivotal role in neuroinflammation and myelin destruction in the central nervous system (CNS) in MS. MicroRNA-29b (MiR-29b) and miR-326 contribute to regulating Th1 and Th17 differentiation and altered expression of the miRNAs could be associated with response to treatment in multiple sclerosis (MS). Therefore, our study aimed to evaluate the percentage of Th1 and Th17 and determining the expression levels of miR-29b-3p and miR-326 in these lymphocyte subpopulations between responsive and non-responsive to interferon beta (IFN-&#x3B2;) therapy in relapsing-remitting multiple sclerosis (RRMS) patients.
The present study was performed on 40 RRMS patients following treatment with IFN-&#x3B2;. The percentage of Th1 cells and Th17 cells were determined by flow cytometry in responsive and non-responsive patients. The expression levels of miR-29b-3p and miR-326 were assessed in Th1 and Th17 cells by quantitative polymerase chain reaction (PCR). Enzyme-linked immunosorbent assay (ELISA) was applied to evaluate the plasma levels of IFN-&#x3B3; and IL-17A.
No significant difference was observed in the percentage of Th1 and Th17 cells as well as the expression levels of miR-29b-3p and miR-326 (in Th1 and Th17, respectively) in treated patients. Also, we did not find any significant difference in IFN-&#x3B3; and IL-17A plasma concentration between responsive or non-responsive to IFN-&#x3B2; therapy in patients with RRMS.
IFN-&#x3B2; may regulate other miRNAs in Th1 and Th17 cells than miR29b-3p and miR-326 in MS patients.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2703</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">Combination of 5-fluorouracil and Lipopolysaccharide Synergistically Induces Cytotoxicity and Apoptosis in MCF-7 Human Breast Cancer Cells</title>
    <FirstPage>426</FirstPage>
    <LastPage>436</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Negin</FirstName>
        <LastName>Nokhandani</LastName>
        <affiliation locale="en_US">Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran AND Department of Immunology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahdieh</FirstName>
        <LastName>Naghavi  Alhosseini</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ali</FirstName>
        <LastName>Memarian</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Homa</FirstName>
        <LastName>Davoodi</LastName>
        <affiliation locale="en_US">Cancer Research Center, Golestan University of Medical Sciences, Gorgan, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>08</Month>
        <Day>11</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>02</Month>
        <Day>15</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Several studies have been conducted to find suitable combinations of drugs to increase the efficacy of chemotherapy and reduce the resistance of tumor cells to treatment. Lipopolysaccharide (LPS), as a ligand for Toll-like receptor 4 (TLR-4), can modify immune responses in different cancers. Although multiple studies have been performed in this area, the effect of LPS on tumor cells remains controversial. In the present study, the cytotoxic effects of 5-fluorouracil (5-FU), with or without LPS, were evaluated in human breast cancer cell line (MCF-7) on apoptosis and gene expression in downstream signaling pathways.
MCF-7 was obtained from the Pasteur Institute of Iran. The effects of LPS and 5-FU on cytotoxicity, apoptosis, and gene expression in NF-&#x3BA;B, ERK, and AKT signaling pathways were evaluated by MTT assay, Annexin V/propidium iodide (PI) apoptosis assay, and qRT-PCR, respectively.
Our findings showed that LPS alone did not significantly affect cytotoxicity or apoptosis, compared to the control cells (untreated cells), while combined with 5-FU, it caused a significant increase in the apoptosis of cancer cells and decreased cell viability. It was also concluded that LPS in combination with 5-FU increased TLR-4 expression and down-regulated gene expression in NF-&#x3BA;B, ERK, and AKT pathways (p=0.001).
Although the role of LPS in tumor inhibition or progression remains controversial, our findings suggest that LPS can be considered a novel complementary approach intranslational oncology research of breast cancer therapy.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2487</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">Increased Expression of B Lymphocyte Induced Maturation Protein 1 (BLIMP1) in Patients with Common Variable Immunodeficiency (CVID)</title>
    <FirstPage>437</FirstPage>
    <LastPage>446</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Shockrollah</FirstName>
        <LastName>Farrokhi</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, Boushehr University of Medical Sciences, Boushehr, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Faezeh</FirstName>
        <LastName>Abbasi-rad</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nafiseh</FirstName>
        <LastName>Esmaeil</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <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>Reza</FirstName>
        <LastName>Yazdani</LastName>
        <affiliation locale="en_US">Research Center for Immunode&#xFB01;ciencies, Pediatrics Center of Excellence, Children's Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sanaz</FirstName>
        <LastName>Afshar-Ghasemlou</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Saba</FirstName>
        <LastName>Fekrvand</LastName>
        <affiliation locale="en_US">Research Center for Immunode&#xFB01;ciencies, Pediatrics Center of Excellence, Children's Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mazdak</FirstName>
        <LastName>Ganjalikhani-Hakemi</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran AND Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>12</Month>
        <Day>07</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>06</Month>
        <Day>11</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Common variable immunodeficiency (CVID) is a primary immune deficiency disorder characterized by a failure in B cell differentiation, impaired immunoglobulin production,and defect in response to vaccines. As a result of defective B cell maturation and differentiation in CVID, the affected patients commonly present with reduced numbers of memory B cell and antibody-secreting plasma cells. B-cell lymphoma 6 protein (BCL6) and B lymphocyte induced maturation protein 1 (BLIMP1) molecules are two important transcription factors that have key roles in the maturation of B cells to plasma cells. Hence, in the current survey, we aimed to evaluate the mRNA and protein expression levels of BCL6 and BLIMP1 in B lymphocytes isolated from peripheral blood in CVID patients.
We collected blood samples from 12 CVID patients and 12 healthy controls. We isolated peripheral blood mononuclear cells (PBMCs) using Ficoll density gradient separation. Then, CD19+ B cells were purified using MACS. The protein expression and transcriptional level of BCL6 and BLIMP1 were respectively measured using flow cytometry and real-time PCR.
Our results showed that the BLIMP1 mRNA expression, as well as BLIMP1 protein expression, were significantly higher in CVID patients compared to control subjects (p=0.009 and p=0.007, respectively). However, we found no significant difference in mRNA and protein expression of BCL6 between patients and healthy controls.
Accord