<?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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Pro and Anti-inflammatory Cytokine Production in CD4+ T Lymphocytes in Children with Asthma and Allergic Rhinitis Exposed to the Monocyte Locomotion Inhibitory Factor (MLIF)</title>
    <FirstPage>388</FirstPage>
    <LastPage>392</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Sara</FirstName>
        <LastName>Rojas-Dotor</LastName>
        <affiliation locale="en_US">Departamento de Salud P&#xFA;blica, Facultad de Medicina Universidad Nacional Aut&#xF3;noma de M&#xE9;xico,&#xA0;M&#xE9;xico City, M&#xE9;xico</affiliation>
      </Author>
      <Author>
        <FirstName>Adriana</FirstName>
        <LastName>Gonz&#xE1;lez-Hern&#xE1;ndez</LastName>
        <affiliation locale="en_US">Unidad de Medicina Familiar No. 7, Instituto Mexicano del Seguro Social, M&#xE9;xico City, M&#xE9;xico</affiliation>
      </Author>
      <Author>
        <FirstName>Francisco</FirstName>
        <LastName>Le&#xF3;n-Aguilar</LastName>
        <affiliation locale="en_US">Unidad de Medicina Familiar No. 7, Instituto Mexicano del Seguro Social, M&#xE9;xico City, M&#xE9;xico</affiliation>
      </Author>
      <Author>
        <FirstName>V&#xED;ctor</FirstName>
        <LastName>Ju&#xE1;rez-T&#xE9;llez</LastName>
        <affiliation locale="en_US">Unidad de Medicina Familiar No. 7, Instituto Mexicano del Seguro Social, M&#xE9;xico City, M&#xE9;xico</affiliation>
      </Author>
      <Author>
        <FirstName>Patricia</FirstName>
        <LastName>G&#xF3;mez de Le&#xF3;n-Cruces</LastName>
        <affiliation locale="en_US">Departamento de Salud P&#xFA;blica, Facultad de Medicina Universidad Nacional Aut&#xF3;noma de M&#xE9;xico,&#xA0;M&#xE9;xico City, M&#xE9;xico</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>08</Month>
        <Day>17</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>12</Month>
        <Day>11</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Entamoeba histolytica produces, in axenic culture, the monocytes locomotion inhibitory factor (MLIF), a oligopeptide with selective anti-inflammatory properties. We evaluated the effect of MLIF on the expression of pro- and anti-inflammatory cytokines in CD4+ T lymphocytes from children with asthma and allergic rhinitis. Twelve children with severe asthma, 12 children with allergic rhinitis and 6 healthy controls were recruited for this study between May and December 2016. CD4+ T cells were cultured for 24 h at 37&#xB0;C, 5% CO2 in the presence of MLIF, 1-phorbol 12-myristate 13-acetate (PMA), MLIF+PMA or RPMI. Interleukin-10 (IL-10), IL-4, interferon gamma (IFN-&#x3B3;) and tumor necrosis factor alpha (TNF-&#x3B1;) expression levels were measured in the supernatants of T-cell cultures using the enzyme-linked immunosorbent assay (ELISA). Pro- and anti-inflammatory cytokines were inhibited by MLIF (IFN-&#x3B3; p=0.0036, TNF-&#x3B1; p&lt;0.001, IL-4 p=0.0082) in asthmatic patients, however IFN-&#x3B3; was not significantly inhibited (NS) in patients with allergic rhinitis when compared to the RPMI group. In CD4+ T cells treated with PMA+MLIF, the expression levels of IFN-&#x3B3;, TNF-&#x3B1; and IL-4 were strongly inhibited (p&lt;0.001, p&lt;0.001 and p&lt;0.0094), compared to PMA treatment alone, for both, rhinitis and asthma. IL-10 expression was not affected by MLIF in neither of the two diseases. We conclude that MLIF alters the pro/anti-inflammatory balance and induces inhibition of IL-4, IFN-&#x3B3; and TNF-&#x3B1;, but does not affect IL-10.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1629</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1629/845</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Evaluation of Interleukin-21, 23 and 27 mRNA Expression and Protein Level in Liver Transplant Patients</title>
    <FirstPage>298</FirstPage>
    <LastPage>307</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Afsoon</FirstName>
        <LastName>Afshari</LastName>
        <affiliation locale="en_US">Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran AND&#xA0;Department of Molecular Genetics, Science and Research, Islamic Azad University, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ramin</FirstName>
        <LastName>Yaghobi</LastName>
        <affiliation locale="en_US">Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Negar</FirstName>
        <LastName>Azarpira</LastName>
        <affiliation locale="en_US">Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Bita</FirstName>
        <LastName>Gerami Zadeh</LastName>
        <affiliation locale="en_US">Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Seyed Ali</FirstName>
        <LastName>Malek Hosseini</LastName>
        <affiliation locale="en_US">Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mojtaba</FirstName>
        <LastName>Darbouy</LastName>
        <affiliation locale="en_US">Department of Molecular Genetics, Science and Research, Islamic Azad University, Fars, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hossein</FirstName>
        <LastName>Karimi</LastName>
        <affiliation locale="en_US">Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>08</Month>
        <Day>29</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>12</Month>
        <Day>30</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Cytokines have prominent roles in activating of different T cells and shifting the immune response, in this study the role of three cytokines (IL-21, IL-23 and IL-27) is investigated in the liver transplant rejection. Three EDTA-treated blood samples were collected from each liver transplanted patient in 1st, 4th and 7th day of post-transplantation. The expression level of the mentioned cytokines was determined using real-time PCR for all samples. Also, the serum levels of cytokines were determined using ELISA tests. In acute rejection (AR) group (51 patients), mRNA expression pattern of IL-21and IL-23 showed a steady increase, but this pattern was converse for IL-27. Our results in non-acute rejection (non-AR) group (54 patients) showed an elevation in day 4 and then a decrease in day 7 for IL-21 and IL-23 genes. This pattern was converse again for IL-27 gene. In comparison between the two groups, in all 3 sampling times the mean of mRNA expression level of IL-21 and IL-23, showed an increase in AR group which this increase was significant for IL-21 in the 3rd (p=0.007) and for IL-23 in 2nd (p=0.048) and 3rd (p=0.049) sampling time, but the pattern of mRNA expression for IL-27 was contrary to the results of IL-21 and IL-23. Furthermore, ELISA technique also, showed the serum level changes the same as cytokines. In this study IL-21 and IL-23 showed pro-inflammatory properties in the liver transplant rejected patients. Also, IL-27 having different expression pattern, showed anti-inflammatory behavior which needs more considerations in future.
&#xD;

&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1628</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1628/849</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Frequency and Pattern of IgE-mediated Sensitization to Aero and Food Allergens in Ahvaz, Province of Khuzestan in Southwestern Iran</title>
    <FirstPage>393</FirstPage>
    <LastPage>397</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Shahrooei</LastName>
        <affiliation locale="en_US">Department of Microbiology and Immunology, Laboratory of Clinical Bacteriology and Mycology, KU Leuven, Leuven, Belgium AND&#xA0;Specialized Immunology Laboratory of Dr. Shahrooei, Sina Medical Complex, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abbas</FirstName>
        <LastName>Fayezi</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, School of Medicine, Ahvaz University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Raheleh</FirstName>
        <LastName>Shokouhi Shoormasti</LastName>
        <affiliation locale="en_US">Immunology, Asthma and Allergy Research Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Faramarz</FirstName>
        <LastName>Zakavi</LastName>
        <affiliation locale="en_US">Specialized Immunology Laboratory of Dr. Shahrooei, Sina Medical Complex, Ahvaz, Iran AND&#xA0;Department of Operative Dentistry, School of Dentistry, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Leila</FirstName>
        <LastName>Golpasand Hagh</LastName>
        <affiliation locale="en_US">Specialized Immunology Laboratory of Dr. Shahrooei, Sina Medical Complex, Ahvaz, Iran AND&#xA0;Department of Periodontics, School of Dentistry, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Johan</FirstName>
        <LastName>Van Eldere</LastName>
        <affiliation locale="en_US">Department of Microbiology and Immunology, Laboratory of Clinical Bacteriology and Mycology, KU Leuven, Leuven, Belgium AND&#xA0;Department of Laboratory Medicine, University Hospitals Leuven, Leuven, Belgium</affiliation>
      </Author>
      <Author>
        <FirstName>Xavier</FirstName>
        <LastName>Bossuyt</LastName>
        <affiliation locale="en_US">Department of Laboratory Medicine, University Hospitals Leuven, Leuven, Belgium AND&#xA0;Department of Microbiology and Immunology, Experimental Laboratory Immunology, KU Leuven, Leuven, Belgium</affiliation>
      </Author>
      <Author>
        <FirstName>Erna</FirstName>
        <LastName>Van Hoeyveld</LastName>
        <affiliation locale="en_US">Department of Laboratory Medicine, University Hospitals Leuven, Leuven, Belgium</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>05</Month>
        <Day>19</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
        <Month>01</Month>
        <Day>16</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Efficient diagnosis of allergy and proper treatment need identification of the causative allergens eliciting clinical symptoms. The present study was performed to identify the most common aero- and food allergens and determine the pattern of sensitization among people of Ahvaz (southwestern Iran), one of the most polluted cities worldwide. Based on the physical examination and medical records, patients were referred to the Allergy laboratory for &#x201C;in vitro&#x201D; IgE determination. Specific and total IgE was determined by the ImmunoCAP system (Thermo Fisher-Phadia, Uppsala, Sweden). A total of 666 consecutive patients (51.1% female) were tested for 202 different allergens. The majority of requests (57%) belonged to food allergens. Sensitization to at least one allergen was found in 47.6% of patients. In a selected group of allergens for which specific IgE had been tested in at least 100 patients, the most common sensitizing aeroallergens were Russian thistle, grass pollen, and willow; while wheat, honey, and shrimp were the most frequent food allergens, respectively. Sensitization profiles based on measurement of specific IgE indicated that Russian thistle, grasses, and wheat were the most prevalent allergens in people with allergic symptoms living in Ahvaz.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1471</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1471/854</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Immunotherapeutic Effects of &#x3B2;-D Mannuronic Acid on IL-4, GATA3, IL-17 and RORC Gene Expression in the PBMC of Patients with Inflammatory Bowel Diseases</title>
    <FirstPage>308</FirstPage>
    <LastPage>317</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Hussaini</FirstName>
        <LastName>Alhassan Mohammed</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, International Campus, Tehran University of&#xA0;Medical Sciences, Tehran, Iran AND&#xA0;Department of Immunology, Faculty of Medical Laboratory Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria</affiliation>
      </Author>
      <Author>
        <FirstName>Ali Akbar</FirstName>
        <LastName>Saboor-Yaraghi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, International Campus, Tehran University of&#xA0;Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Homayoun</FirstName>
        <LastName>Vahedi</LastName>
        <affiliation locale="en_US">Digestive Disease Research Institute, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ghordratollah</FirstName>
        <LastName>Panahi</LastName>
        <affiliation locale="en_US">Department of Medical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Gholamreza</FirstName>
        <LastName>Hemmasi</LastName>
        <affiliation locale="en_US">Department of Internal Medicine and Gastroenterology, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mir Saeed</FirstName>
        <LastName>Yekaninejad</LastName>
        <affiliation locale="en_US">Department of Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abbas</FirstName>
        <LastName>Mirshafiey</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, International Campus, Tehran University of&#xA0;Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>07</Month>
        <Day>13</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>08</Month>
        <Day>09</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Inflammatory bowel diseases (IBD) are chronic relapsing immune-mediated disorders that result from an aberrant immunological response. IBD comprises of Crohn's disease (CD) and ulcerative colitis (UC). The precise aetiology of IBD has not been fully understood, however, recent studies support the hypothesis that patients with IBD have a dysregulated immune response to endogenous bacteria in the gastrointestinal tract (GIT). The increasing number of hospitalisation coupled with the high economic burden faced by IBD patients, calls for more concerted research efforts, to design a potent and credible treatment option for these strata of patients. This research was designed to test the efficacy and potency of &#x3B2;-D Mannuronic acid (M2000) in the treatment of IBD. Ten ml of blood was aseptically collected from 24 IBD patients and 24 normal controls. PBMC was isolated and stimulated with 1 &#xB5;g/mL of LPS and incubated for 4 hours. The cells were later treated with 10 &#xB5;g/mL or 50 &#xB5;g/mL of Mannuronic acid and incubated for 24 hours at 370C under 5% CO2 and 100% humidity. After the incubation, RNA was extracted from the cells, cDNA was synthesised, and the expression of the gene was evaluated using quantitative real-time PCR. The result indicated a significant down-regulation of RORC and IL-17 genes expression, while the expression of IL-4 and GATA3 genes were significantly up-regulated. These research findings have shown that M2000 a biocompatible agent, that has an immunotherapeutic, immunomodulatory and immunosuppressive effects on the PBMC of IBD patients.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1564</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1564/850</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Mir-22-3p Enhances the Chemosensitivity of Gastrointestinal Stromal  Tumor Cell Lines to Cisplatin through PTEN/PI3K/Akt Pathway</title>
    <FirstPage>318</FirstPage>
    <LastPage>325</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Yugang</FirstName>
        <LastName>Xu</LastName>
        <affiliation locale="en_US">Department of General Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China&#xA0;AND&#xA0;Department of General Surgery, Tai'an Central Hospital, Tai'an, Shandong, China</affiliation>
      </Author>
      <Author>
        <FirstName>Ming</FirstName>
        <LastName>Cheng</LastName>
        <affiliation locale="en_US">Department of General Surgery, Tai'an Central Hospital, Tai'an, Shandong, China</affiliation>
      </Author>
      <Author>
        <FirstName>Lei</FirstName>
        <LastName>Mi</LastName>
        <affiliation locale="en_US">Department of General Surgery, Tai'an Central Hospital, Tai'an, Shandong, China</affiliation>
      </Author>
      <Author>
        <FirstName>Yunping</FirstName>
        <LastName>Qiu</LastName>
        <affiliation locale="en_US">Department of General Surgery, Tai'an Central Hospital, Tai'an, Shandong, China</affiliation>
      </Author>
      <Author>
        <FirstName>Wenli</FirstName>
        <LastName>Hao</LastName>
        <affiliation locale="en_US">Department of General Surgery, Tai'an Central Hospital, Tai'an, Shandong, China</affiliation>
      </Author>
      <Author>
        <FirstName>Leping</FirstName>
        <LastName>Li</LastName>
        <affiliation locale="en_US">Department of General Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>08</Month>
        <Day>11</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>12</Month>
        <Day>05</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Mir-22-3p is associated with many important biological processes, including neuroprotection, tumorigenesis, and various other tumor progressions. Our study aimed to investigate the roles of Mir-22-3p in chemosensitivity of gastrointestinal stromal tumor (GIST-T1) cells to cisplatin and explore its underlying mechanisms. Mir-22-3p high-expressing cell line was established by transfecting GIST-T1 cell line cells with Mir-22-3p mimic. After treatment with cisplatin (10 &#x3BC;M), Cell counting kits-8 (CCK-8) method was used to detect the cell viability. Flow cytometry was applied to measure the degree of cell apoptosis. Scratch wound healing test was used to detect the migration ability of cells. The protein and mRNA levels of the phosphatase and tensin homolog deleted on chromosome ten (PTEN)/phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) pathway-related factors were analyzed by Western blot and qRT-PCR. The mRNA level of Mir-22-3p was increased in transfected GIST-T1 cells compared with that in control cells. The survival rate and Bcl-2/Bax ratio of GIST-T1 cells treated with both Mir-22-3p analogue and cisplatin were significantly decreased, while the apoptosis rate and protein level of caspase-3 were significantly increased (p&lt;0.05). In addition, the mRNA and protein levels of PTENwere significantly increased in cells treated with both Mir-22-3p analogue and cisplatin (p&lt;0.05), while the expression levels of PI3K and Akt were significantly decreased (p&lt;0.05). Mir-22-3p overexpression can increase the chemosensitivity of cisplatin in human gastrointestinal stromal tumor cells by PTEN/PI3K/Akt pathway.&#xA0;&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1622</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1622/851</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Quantum Dot-labeled Tags Improve Minimal Detection Limit of CA125 in Ovarian Cancer Cells and Tissues</title>
    <FirstPage>326</FirstPage>
    <LastPage>335</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Sorour</FirstName>
        <LastName>Shojaeian</LastName>
        <affiliation locale="en_US">Department of Biochemistry, Medical Genetics, Nutrition, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abdolamir</FirstName>
        <LastName>Allameh</LastName>
        <affiliation locale="en_US">Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahmood</FirstName>
        <LastName>Jeddi-Tehrani</LastName>
        <affiliation locale="en_US">Department of Hybridoma, Monoclonal Antibody Research Center, Avicenna Research Institute, Academic Center for Education, Culture and Research (ACECR), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Roya</FirstName>
        <LastName>Ghods</LastName>
        <affiliation locale="en_US">Oncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran AND Department of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medicine Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Jaleh</FirstName>
        <LastName>Shojaeian</LastName>
        <affiliation locale="en_US">University of Maryland School of Pharmacy, Baltimore, Maryland,&#xA0;USA</affiliation>
      </Author>
      <Author>
        <FirstName>Akram-Sadat</FirstName>
        <LastName>Tabatabaei-Panah</LastName>
        <affiliation locale="en_US">Department of Biology, Faculty of Basic Sciences, Islamic Azad University, East Tehran Branch&#xA0;(Ghiamdasht), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Amir-Hassan</FirstName>
        <LastName>Zarnani</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran AND&#xA0;Reproductive Immunology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran AND&#xA0;Immunology Research Center (IRC), Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>08</Month>
        <Day>01</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
        <Month>02</Month>
        <Day>13</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">In recent years, a lot of attention has been paid to quantum dot (QD) nanoparticles as fluorescent sensors for sensitive and accurate detection of cancer biomarkers. Here, using a homemade specific monoclonal antibody against CA125 and QD525- or FITC-labeled probes, expression of this marker in an ovarian cancer cell line and cancer tissues were traced and optical properties of fluorophores were compared qualitatively and quantitatively. Our results clearly showed that besides lower background and exceptionally higher photobleaching resistance, QD525 exhibited higher fluorescent intensity for both ovarian cancer cell and tissues at different exposure times (p&lt;0.0001) and excitation filter sets (p&lt;0.0001) exemplified by significantly higher staining index (p&lt;0.016). More importantly, the FITC-labeled probe detected antigen-antibody complex at minimum concentration of 0.3 mg/mL of anti-CA125, while reactivity limit decreased to 0.078 mg/mL of anti-CA125 when QD525-labeled probe was applied showing four times higher reactivity level of QD525 probe compared to the same probe labeled with FITC. Based on our results, it seems that QDs are inimitable tags for sensitive detection and localization of ovarian cancer micrometastasis and molecular demarcation of cancer tissues in surgical practice, which subsequently figure out accurate therapeutic approaches.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1603</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1603/840</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Sex Hormones and Prolactin Levels and Their Association with Anti Cardiolipin Antibody in Patients with Systemic Lupus Erythematosus</title>
    <FirstPage>336</FirstPage>
    <LastPage>345</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Dariyush</FirstName>
        <LastName>Raeisi</LastName>
        <affiliation locale="en_US">Department of Internal Medicine, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Erfan</FirstName>
        <LastName>zare</LastName>
        <affiliation locale="en_US">Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Atefeh</FirstName>
        <LastName>Nasir Kansestani</LastName>
        <affiliation locale="en_US">Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran AND&#xA0;Nosocomial Infection Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamidraza</FirstName>
        <LastName>Sherkatolabbasieh</LastName>
        <affiliation locale="en_US">Department of Pediatric, Lorestan University of Medical Sciences, khorramabad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Shiva</FirstName>
        <LastName>Shafeizadeh</LastName>
        <affiliation locale="en_US">Department of Internal Medicine, Lorestan University of Medical Sciences, khorramabad, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>04</Month>
        <Day>26</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>10</Month>
        <Day>02</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Pathogenesis of systemic lupus erythematosus (SLE) is complex and multi-factorial. Among various suggested mechanisms for the disease, the hormonal theory has been considered as one of the most important mechanisms. Recently, the association of sex hormones with manifestations of antiphospholipid antibody syndrome (APLS) has been hypothesized. The aim of present study was to assess the serum levels of anticardiolipin antibody (ACA), sex hormones and prolactin in SLE female patients and their association with the disease. This study comprised 40 SLE female patients and 41 healthy age-matched female subjects. For all patients and controls, the serum levels of ACA (IgG and IgM), estradiol, testosterone, progesterone, dehydroepiandrosterone sulfate (DHEA-S) and prolactin were measured by ELISA method. Our study revealed that serum levels of testosterone, DHEA-S and progesterone were significantly lower in SLE patients than control (p&lt;0.001). However, serum levels of estradiol and prolactin were significantly higher in SLE patients compared to controls (p&lt;0.001). There was a significant difference between mild and moderate severity patients group for ACA positivity (95% CI 13.67-41.3; p=0.03). Also, SLE patients with positive ACA showed significantly lower (p&lt;0.001) serum levels of testosterone, DHEA-S and progesterone and significantly higher (p&lt;0.001) estradiol and prolactin serum levels compared to negative ACA patients. The results of our study indicated that expression and metabolism of sex hormones and prolactin are different in female SLE patients compared to healthy subjects. It seems, change in serum levels of these hormones is related to higher SLE disease activity, increased thrombotic risks and increased renal involvement.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1435</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1435/852</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Characterization of CD4+ and CD8+ T Cell Subsets and Interferon Regulatory Factor 4 (IRF4) in MS Patients Treated with Fingolimod (FTY-720): A Follow-up Study</title>
    <FirstPage>346</FirstPage>
    <LastPage>360</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Bahare</FirstName>
        <LastName>Laribi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Ali</FirstName>
        <LastName>Sahraian</LastName>
        <affiliation locale="en_US">MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehdi</FirstName>
        <LastName>Shekarabi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Rahimeh</FirstName>
        <LastName>Emamnejad</LastName>
        <affiliation locale="en_US">Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohsen</FirstName>
        <LastName>Marzban</LastName>
        <affiliation locale="en_US">Department of Neurosciences, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Shokufeh</FirstName>
        <LastName>Sadaghiani</LastName>
        <affiliation locale="en_US">MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Izad</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND&#xA0;MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>08</Month>
        <Day>01</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>08</Month>
        <Day>27</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Fingolimod is a novel immunomodulatory drug used in patients with relapsing multiple sclerosis (MS) which reversibly inhibits egress of lymphocytes from lymph nodes. In this longitudinal study, the frequency of Interferon- gamma (IFN-&#x3B3;)+, IL4+, IL17+ and IL10+ CD4+ and CD8+ T cell subsets were measured in Fingolimod treated patients before and after 12 months&#x2019;(12M) therapy using flow cytometry and compared to those of naive, Betaferon treated MS patients and healthy individuals. Additionally, the level of transcription factor IRF4 and IL-6, IL-23, TGF-&#x3B2;1 cytokines, required for differentiation of IL-17+ T cells, were assessed by RT-PCR and ELISA, respectively. In Fingolimod treated MS patients, we observed a significant decrease in the percentage of IFN-&#x3B3;+/IL17+ CD4+ and CD8+ T cell subsets. In contrast, Fingolimod increased IL10+ CD4+ T cells. We also showed that IFN-&#x3B3;+IL17+ co-producing CD8+ T cells were reduced in patients under &#xFB01;ngolimod therapy. furthermore, Fingolimod could reduce the expression level of IRF4 in patients while IL6 was increased in the supernatant of cultured peripheral blood mononuclear cells. Our data showed that Fingolimod treatment alters CD4+ and CD8+ T cell subsets and reduces expression of IRF-4, which affects the proportion of pathogenic memory T cells in peripheral blood.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1601</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1601/842</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Collagen II-primed Foxp3 Transduced T Cells Ameliorate  Collagen-induced Arthritis in Rats: The Effect of Antigenic  Priming on T Regulatory Cell Function</title>
    <FirstPage>361</FirstPage>
    <LastPage>371</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Mahdi</FirstName>
        <LastName>Zavvar</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohsen</FirstName>
        <LastName>Abdolmaleki</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamid</FirstName>
        <LastName>Farajifard</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Farshid</FirstName>
        <LastName>Noorbakhsh</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>kayhan</FirstName>
        <LastName>Azadmanesh</LastName>
        <affiliation locale="en_US">Department of Virology, Pasteur Institute of Iran, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Vojgani</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hossein</FirstName>
        <LastName>Nikcnam</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND&#xA0;Molecular Immunology Research Center, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>08</Month>
        <Day>05</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>12</Month>
        <Day>18</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Regulatory T cells (Tregs) play a major role in the prevention of autoimmune diseases. Transfer of Foxp3 gene into conventional T cells converts their phenotype to regulatory T cells. Therefore, the question arises as to whether adoptively transferred in vitro differentiated Treg cells specific for a locally expressed antigen might have better inhibitory effects on the progression of the disease as compared with antigen-nonspecific T reg cells. Herein, we investigated the therapeutic potential of primed and unprimed retrovirus mediated Foxp3-overexpression T cells following intravenously injected of these cells into affected rats with collagen-induced arthritis (CIA), an animal model of rheumatoid arthritis. Our analyses demonstrate that systemic administration of collagen II primed Foxp3-transduced T cells could markedly ameliorate CIA inflammatory responses at clinical (p&lt;0.0014) and pathological exchanges including cellular infiltration (p=0.002), bone erosion (p=0.0013) and synovial hyperplasia (p=0.002). In contrast, collagen II unprimed Foxp3-transduced T cells like as collagen II primed or unprimed GFP-transduced T cells did not reveal any beneficial effects on arthritis features as compared with untreated group (p&gt;0.05). Therefore, we believe that collagen II primed Foxp3-transduced T cells are interacting locally and systemically with immune cells which reveled with decreasing of T cells infiltration into joints along with specific CII IgG production. Considering the results described here, it appears that the using patients' T cells which previously exposed to specific antigens may have more effective therapeutic advantage in the production of induced regulatory T cells in the treatment of arthritis.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1609</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1609/853</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Nicotine Modulates the Release of Inflammatory Cytokines and Expression of TLR2, TLR4 of Cord Blood Mononuclear Cells</title>
    <FirstPage>372</FirstPage>
    <LastPage>378</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Laya</FirstName>
        <LastName>Takbiri Osgoei</LastName>
        <affiliation locale="en_US">Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Kazem</FirstName>
        <LastName>Parivar</LastName>
        <affiliation locale="en_US">Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Marzieh</FirstName>
        <LastName>Ebrahimi</LastName>
        <affiliation locale="en_US">Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell&#xA0;Biology and Technology, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Esmaeil</FirstName>
        <LastName>Mortaz</LastName>
        <affiliation locale="en_US">Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis&#xA0;and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran AND&#xA0;Department of Immunology, Faculty of Medicine, Shahid Beheshti University of&#xA0;&#xA0;Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>06</Month>
        <Day>13</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>09</Month>
        <Day>19</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">The underlying mechanisms of how nicotine affects cord umbilical cells remain largely elusive. Nicotine rapidly crosses the blood-brain barrier (10 to 20 s) and binds to nicotinic acetylcholine receptors (nAChRs). Nicotine considered as a major compound found in cigarette smoke and the mechanism of nicotine action in immune response is not well understood. Cigarette smoke well known by activation of toll like receptors (TLRs) especially TLR4 and 9 which stimulates the immune response by induction of releases of cytokines mainly CXCL-8 which in turn triggers lungs reactions specially induction of neutrophils recruitments. In this study we isolated human umbilical mononuclear cells (UCBMC) from umbilical cord blood and exposed to the nicotine for detection any cytokines and TLRs modulation. We have found that nicotine (at concentration 0.01&#xB5;M) induced release of TNF-a and IL-6 but not CXCL-8 production. Besides we have shown that nicotine did not effect on TLR4 surface expression however up-regulated the TLR2 surface expression. Moreover expression of CD11a and CXCR4 after nicotine incubation was upregulated as demonstrated by flow cytometry analysis, These data indicated that nicotine by stimulation of inflammatory cytokines induces immune response. The present study provides evidence that nicotine selectively regulates the release of cytokines and expression of TLRs. Further studies are needed to exploring details of its effects and signaling.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1509</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1509/839</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>17</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="epublish">
        <Year>2018</Year>
        <Month>08</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Evaluation of mRNA Expression Levels of TNF&#x3B1;, TNFR1 and IL1&#x3B2; in Lung Tissue 20 Years after Sulfur-mustard Exposure</title>
    <FirstPage>379</FirstPage>
    <LastPage>387</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Marzieh</FirstName>
        <LastName>Eghtedardoost</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zuhair</FirstName>
        <LastName>Hassan</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Tooba</FirstName>
        <LastName>Ghazanfari</LastName>
        <affiliation locale="en_US">Immunoregulation Research Center, Shahed University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Alireza</FirstName>
        <LastName>Sadeghipour</LastName>
        <affiliation locale="en_US">Pathology Department, Rasoul Akram Medical Complex, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mostafa</FirstName>
        <LastName>Ghanei</LastName>
        <affiliation locale="en_US">Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran AND&#xA0;Department of Respiratory, Pasteur Institute of Iran, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2017</Year>
        <Month>07</Month>
        <Day>22</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>09</Month>
        <Day>13</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Despite many years having passed since exposure to sulfur mustard (SM) gas, there are many exposed subjects who are still suffering from delayed pulmonary complications. The levels of pro-inflammatory cytokines in the lung of these subjects have not been investigated in delay phase. In this study, we evaluated mRNA expression of pro-inflammatory &#xA0;cytokines (tumor necrosis factor alpha (TNF&#x3B1;), tumor necrosis factor receptor type 1 (TNFR1), and interleukin 1 beta (IL-1&#x3B2;) &#xA0;) in lung biopsy of SM-exposed subjects and compared them with control (non-exposed) subjects. We used formalin-fixed, paraffin-embedded (FFPE) tissue for this purpose. Lung FFPE blocks of SM-exposed subjects (30 samples) and a control group (30 samples) were collected from archival pathology department. The total mRNA of FFPE tissues were extracted and the mRNA expression of pro-inflammatory &#xA0;cytokines were determined by quantitative Real Time PCR (RT-qPCR). The obtained results from two groups were compared to each other and non-parametric statistical analyses were carried out on them. Our studies showed that the mRNA expression of TNF&#x3B1;, TNFR1 and IL-1&#x3B2; &#xA0;in lung tissue of SM injured and control people have no significant difference (p-value= 0.159, 0.832 and 0.314 respectivly). TNFR1 showed direct correlation with TNF&#x3B1; (r=0.867, p=0.002) and IL-1&#x3B2; (r= 0.65, p=0.006). The evaluation of mRNA expression in pro-inflammatory cytokines in lung of SM-exposed subjects after 20 years showed that these mediators are similar to those of non-exposed group and there was no acute inflammation in lung of these patients.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1582</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1582/841</pdf_url>
  </Article>
</Articles>
