<?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>16</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2017</Year>
        <Month>02</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Human Leukocyte Antigen (HLA) Class I and II Polymorphism in Iranian Healthy Population from Yazd Province</title>
    <FirstPage>1</FirstPage>
    <LastPage>13</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Behrouz</FirstName>
        <LastName>Nikbin</LastName>
        <affiliation locale="en_US">Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran AND&#xA0;Immunogenetic Laboratory, Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hossein</FirstName>
        <LastName>Nicknam</LastName>
        <affiliation locale="en_US">Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran AND&#xA0;Immunogenetic Laboratory, Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hossein</FirstName>
        <LastName>Hadinedoushan</LastName>
        <affiliation locale="en_US">Department of Immunology, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Bita</FirstName>
        <LastName>Ansaripour</LastName>
        <affiliation locale="en_US">Immunogenetic Laboratory, Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Batol</FirstName>
        <LastName>Moradi</LastName>
        <affiliation locale="en_US">Immunogenetic Laboratory, Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mirsaeed</FirstName>
        <LastName>Yekaninejad</LastName>
        <affiliation locale="en_US">Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahdi</FirstName>
        <LastName>Aminikhah</LastName>
        <affiliation locale="en_US">Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Mehdi</FirstName>
        <LastName>Ranjbar</LastName>
        <affiliation locale="en_US">Department of Immunology, Razi Vaccine and Serum Research Institute, Karaj, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Aliakbar</FirstName>
        <LastName>Amirzargar</LastName>
        <affiliation locale="en_US">Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran AND&#xA0;Immunogenetic Laboratory, Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>12</Month>
        <Day>23</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>08</Month>
        <Day>08</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">The major histocompatibility complex (MHC) genes are the most polymorphic loci in the human genome and have been widely studied in various populations and ethnic groups. Investigations into the HLA genes and proteins have been useful tool for anthropological, transplantation and disease association studies. The polymorphism of the HLA class I (A, B, C) and class II (DRB1, DQA1, DQB1) genes were investigated in 90 unrelated Iranian individuals from Yazd province located in the center of Iran using sequence-specific primers (PCR-SSP). Allele and haplotype frequencies, expected/observed heterozygosity, unbiased expected heterozygosity, number of effective alleles, deviations from Hardy-Weinberg (HW) equilibrium and genetic diversity were computed. A total of 23, 48, 23, 24, 13 and 16 alleles for HLA-A, -B,-C, -DRB1, -DQA and -DQB loci were determined, respectively in the population study. The most frequent allele identified in this study were A*02:01 (18.889%), HLA-B* 51:01 (12.778%), HLA-C* 12:03 (17.033%), HLA-DRB* 11 (24.4%), HLA-DQA* 05:05 (20.55%) and HLA-DQB*03:01 (22.8%).Furthermore, the most frequent 3-locus haplotypes were DRB*11-DQA*05:01-DQB*03:01 (21.1%), HLA-A*02:01- B *50:01- DRB*07:01 (4.9%) and A*26:01 &#x2013;B* 38:01 &#x2013;C*12:03(5%). The most 4-locus haplotype were A*11:01 &#x2013;B* 52:01 &#x2013;C*12:03 &#x2013;DRB!*15(2.5%) and A*02:01 &#x2013;B* 50:01 &#x2013;DRB1*07:01 &#x2013;DQB1*02:01(4.5%). The heterozygosity of the study population was confirmed the expected value and not deviated from Hardy-Weinberg equilibrium for all loci (p&gt;0.05). Our study shows a close relatedness between Yazd population and other ethnic group of Iran despite some differences, which may be due to admixture of each one of these groups with each other or foreigner subpopulations during centuries. Moreover, the results of this study suggest that the Iranian population from Yazd province is in close vicinity with the Caucasians populations and far from the Korean and Japanese populations.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/745</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/745/701</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>16</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2017</Year>
        <Month>02</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Effects of Submaximal Aerobic Exercise on Regulatory T Cell Markers of Male Patients Suffering from Ischemic Heart Disease</title>
    <FirstPage>14</FirstPage>
    <LastPage>20</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Fariba</FirstName>
        <LastName>Raygan</LastName>
        <affiliation locale="en_US">Department of Cardiology, Kashan University of&#xA0;Medical Sciences, Kashan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mansour</FirstName>
        <LastName>Sayyah</LastName>
        <affiliation locale="en_US">Trauma Research Center, Kashan University of&#xA0;Medical Sciences, Kashan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Seyed Mohammad Reza</FirstName>
        <LastName>Janesar Qamsari</LastName>
        <affiliation locale="en_US">Student Research Center, Kashan University of&#xA0;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>Mojtaba</FirstName>
        <LastName>Sehat</LastName>
        <affiliation locale="en_US">Department of Community Medicine, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2016</Year>
        <Month>05</Month>
        <Day>21</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2017</Year>
        <Month>01</Month>
        <Day>17</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">There are confirmed beneficiary effects of exercise on atherosclerotic inflammation of ischemia-associated heart diseases. The purpose of this study was to evaluate the effect of aerobic exercise on T-regulatory cell markers of IL-35 as well as FoxP3 and T-helper2 marker of IL-33 in patients with ischemic heart disease (IHD). This research was performed on 44 asymptomatic male patients with ischemic heart disease. The participants were randomly assigned into two groups of submaximal aerobic exercise and control group. Blood samples were collected before and after the termination of the exercise protocol. Serum levels of IL-35 and IL-33 as well as the amount of FoxP3 gene expression in peripheral blood mononuclear cells were measured by Elisa and Real time PCR, respectively. Serum levels of IL-35 (p=0.001) as well as the amount of FoxP3 gene expression increased significantly (p=0.012)&#xA0; in exercise group even after controlling the likely confounding effects of age, length of ischemia, duration of the disease, and the amount of such factors before exercise (p&#x2264;0.042). It seems that exercise may yield a better control of atherosclerotic inflammation in patients with ischemic heart disease through the induction of regulatory T cells.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/923</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/923/704</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>16</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2017</Year>
        <Month>02</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Inverse Relation between MxA Gene Expression and Age in Multiple Sclerosis Patients Reveals a Gender Difference in Response to Interferon Therapy</title>
    <FirstPage>21</FirstPage>
    <LastPage>27</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Taheri</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammadreza</FirstName>
        <LastName>Mirinezhad</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mir Davood</FirstName>
        <LastName>Omrani</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Elham</FirstName>
        <LastName>Sajjadi</LastName>
        <affiliation locale="en_US">Department of Hematology, School of Paramedical Sciences, Shahid Beheshti University&#xA0;of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hidetoshi</FirstName>
        <LastName>Inoko</LastName>
        <affiliation locale="en_US">Department of Molecular Life Science, Tokai University School of Medicine, Isehara, Japan&#xA0;AND&#xA0;Genodive Pharma Inc., Atsugi, Japan</affiliation>
      </Author>
      <Author>
        <FirstName>Arezou</FirstName>
        <LastName>Sayad</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2016</Year>
        <Month>03</Month>
        <Day>31</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>08</Month>
        <Day>02</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Multiple sclerosis (MS) is an inflammatory, multifocal, immune-mediated disease of the central nervous system that women are at a higher risk to acquire than men. Myxovirus resistance protein A (MxA) is used as a predictive marker of bioactivity of interferon-beta (IFN-&#x3B2;) therapy in MS patients. This study was undertaken in west of Iran to investigate gender differences in the expression level of MxA in relapsing-remitting MS (RRMS) patients receiving IFN-&#x3B2; therapy, compared with untreated normal individuals. The expression level of the MxA gene in RRMS samples were compared to untreated normal individuals using the extracted RNA from whole blood of 50 RRMS patients (31 females and 19 males) and 50 normal controls (29 females and 21 males). All patients were HLA-DRB1*15 negative and responded to IFN-&#x3B2; with a normal vitamin D level. The level of MxA gene expression was measured by quantitative RT-PCR. The levels of gene expression were decreased in RRMS patients compared with normal counterparts (p=0.025). This decrease was significant in females (p=0.009) compared to males (p&gt;0.05). The level of expression varied across different female age-groups with no significant difference in women younger than 30 years, but a significant decrease in expression in women between 30 to 40 years or above 40 years of age was seen. There was neither linear correlation between the MxA expression level and risk of expanded disability status scale of Kurtzke (EDSS); nor were there any significant correlation between expression status of MxA and duration of the disease. In conclusion, the decrease in the level of MxA expression in MS patients treated with IFN-&#x3B2; when compared to normal individuals was significantly lower in females than males.&#xA0; This demonstrated a gender bias in the response to IFN-&#x3B2; therapy that will need to be confirmed and further investigated in more detail.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/859</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/859/693</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>16</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2017</Year>
        <Month>02</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Anti-inflammatory Effects of Novel Thiazolidinone Derivatives as Bioactive Heterocycles on RAW264.7 Cells</title>
    <FirstPage>28</FirstPage>
    <LastPage>38</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Hossein</FirstName>
        <LastName>Ghafoori</LastName>
        <affiliation locale="en_US">Department of Biology, University of Guilan, Rasht, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehrnaz</FirstName>
        <LastName>Rezaei</LastName>
        <affiliation locale="en_US">Department of Biology, University of Guilan, University Campus 2, Rasht, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Asadollah</FirstName>
        <LastName>Mohammadi</LastName>
        <affiliation locale="en_US">Department of Chemistry, University of Guilan, Rasht, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2016</Year>
        <Month>05</Month>
        <Day>04</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>09</Month>
        <Day>04</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">The inhibition of the inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX-2) and nuclear factor-&#x3BA;B (NF-&#x3BA;B) production are research targets of attract in the field of anti-inflammatory drug development. Therefore, this study&#xA0;was designed to investigate the&#xA0;anti-inflammatory effects of novel thiazolidinone derivatives using a cellular model of lipopolysaccharide (LPS)-stimulated murine macrophage RAW 264.7. In the present study,&#xA0;five&#xA0;new&#xA0;derivatives&#xA0;(A to E) of thiazolidinone were synthesized and screened for anti-inflammatory activities. Cell viability of LPS-stimulated RAW 264.7 macrophages clearly decreased in &gt;55 &#x3BC;g/mL of synthesized A-E compounds especially in the presence of C; therefore, up to 50 &#x3BC;g/mL of compounds were selected for the subsequent analysis. A majority of these compounds showed significant inhibition on the production of NO in LPS-stimulated macrophages in a dose-dependent manner. Compounds B and D (10-50 &#x3BC;g/mL) significantly inhibited LPS-induced NF-&#x3BA;B (p65) production in a dose-dependent manner. The effects of B and D on iNOS and COX-2 mRNA and protein expression in LPS-stimulated RAW 264.7 cells were detected by real time-PCR and western blot. B derivative significantly suppressed the iNOS and COX-2 mRNA level and as well as protein expression. Taken together, these results reveal that compound B as new thiazolidinone derivative decreased expression of the inflammatory-related signals (NO, iNOS and COX-2) through regulation of NF-&#x3BA;B; hence, this compound could be suggested as a novel therapeutic strategy for inflammation-associated disorders.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/907</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/907/705</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>16</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2017</Year>
        <Month>02</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">A Real Life Comparison between Allergenic Extracts and Allergenic Molecules</title>
    <FirstPage>39</FirstPage>
    <LastPage>44</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Giorgio</FirstName>
        <LastName>Ciprandi</LastName>
        <affiliation locale="en_US">Allergy Department, Istituto di Ricovero e Cura a Carattere Scientifico &#x2013; Azienda Ospedaliera-Universitaria (IRCCS-AOU), San Martino, Genoa, Italy</affiliation>
      </Author>
      <Author>
        <FirstName>Paola</FirstName>
        <LastName>Comite</LastName>
        <affiliation locale="en_US">Department of Laboratory Medicine, IRCCS-AOU San Martino, Genoa, Italy</affiliation>
      </Author>
      <Author>
        <FirstName>Francesca</FirstName>
        <LastName>Ferrero</LastName>
        <affiliation locale="en_US">Department of Laboratory Medicine, IRCCS-AOU San Martino, Genoa, Italy</affiliation>
      </Author>
      <Author>
        <FirstName>Michele</FirstName>
        <LastName>Mussap</LastName>
        <affiliation locale="en_US">Department of Laboratory Medicine, IRCCS-AOU San Martino, Genoa, Italy</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2016</Year>
        <Month>04</Month>
        <Day>04</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>06</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Serum IgE assay is a mainstay step in the allergy work up. Allergenic extracts and molecular components are available at present. This real life study compared the serum specific IgE levels against allergenic extracts with allergenic molecules in patients allergic to Parietaria, Betulaceae, and mites. This retrospective real life study included 489 subjects with respiratory allergy. Inclusion criteria were 1) documented diagnosis of allergic rhinitis (AR) and/or allergic asthma, and 2) documented allergy to Parietaria judaica (Par j) 2 (216 patients: 112 females, mean age 42 years), or to Betula verrucosa (Bet v) 1 (62 patients: 35 females, mean age 3 years), or Dermatophagoides pteronyssinus (Der p) 1 (211 patients: 107 females, mean age 34 years); and mono-allergy. Serum IgE, specific both for total/crude allergen extracts and individual purified/recombinant allergens, were assessed by ImmunoCap system. The serum IgE levels to birch extract were very strongly (R2=0.96) related to IgE to Bet v 1. There was a strong (R2=0.71) correlation between Dermatophagoides pteronyssinus IgE and Der p 1. A very strong (R2=0.87) correlation also existed between Parietaria extract IgE and Par j 2 IgE levels. However, there was discrepancy between percentages of positivity between allergenic extracts and molecules. Therefore, allergen molecular diagnostics may represent a useful way in allergy work up, but deserves caution in particular circumstances.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/872</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/872/695</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>16</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2017</Year>
        <Month>02</Month>
        <Day>25</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Cow&#x2019;s Milk Desensitization in Anaphylactic Patients: A New Personalized-dose Method</title>
    <FirstPage>45</FirstPage>
    <LastPage>52</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Delara</FirstName>
        <LastName>Babaie</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Mofid Children's Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Nabavi</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Saba</FirstName>
        <LastName>Arshi</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehrnaz</FirstName>
        <LastName>Mesdaghi</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Mofid Children's Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zahra</FirstName>
        <LastName>Chavoshzadeh</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Mofid Children's Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hasan</FirstName>
        <LastName>Bemanian</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mitra</FirstName>
        <LastName>Tafakori</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Mofid Children's Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehrdad</FirstName>
        <LastName>Amirmoini</LastName>
        <affiliation locale="en_US">Department of Allergy and Clinical Immunology, Mofid Children's Hospital, Shahid Beheshti University of </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>11</Month>
        <Day>08</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>01</Month>
        <Day>25</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">One of the inflammatory mediators which is secreted by inflammatory cells is high-mobility group protein B1 (HMGB1). Interaction of HMGB1 and toll-like receptors (TLRs) leads to increased production of inflammatory cytokines. On the other hand, it was shown that triggering receptor expressed on myeloid cells (TREM-1) also can be activated by TLRs, and its soluble form (sTREM-1) can be formed by cleaving of membrane-bound form of TREM-1 proteinases. Since there is not enough knowledge about the precise role of HMGB1 and sTREM-1 in periodontal diseases, the aim of this study was to evaluate the concentration of HMGB1 and sTREM-1 in gingival crevicular fluid (GCF) samples of patients with chronic periodontitis. Gingival crevicular fluid (GCF) samples were obtained from a total of 24 individuals with clinically healthy gingiva and 24 patients with moderate to severe chronic periodontitis. For collecting GCF samples, periopapers were placed at the entrance of the crevice and left in position for 30 seconds. Then, they were stored at -80&#xB0;C. Enzyme-linked immunosorbent assay (ELISA) was used for measuring the concentration of HMGB1 and sTREM-1 in GCF samples. The concentration of HMGB1 (p&lt;0.001) and sTREM-1 (p&lt;0.017), was significantly higher in chronic periodontitis group. In addition, there was a significant positive correlation between HMGB1 and sTREM-1 concentration in chronic periodontitis group (p&lt;0.05). We also found significant positive correlation between PD (Pocket depth) and the concentration of HMGB1 (p&lt;0.001) and sTREM-1 (p&lt;0.015). It is concluded that both HMGB1 and sTREM-1 are released during the inflammatory response of periodontal tissues and they can promote inflammatory process, which leads to tissue destruction.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/664</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/664/666</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>15</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2016</Year>
        <Month>10</Month>
        <Day>31</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">T-helper Cell Type-1 Transcription Factor T-Bet  Is Down-regulated in Type 1 Diabetes</title>
    <FirstPage>386</FirstPage>
    <LastPage>393</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Hajar</FirstName>
        <LastName>Vaseghi</LastName>
        <affiliation locale="en_US">Department of Biology, Faculty of Biological Sciences, Gonbad Kavous University,&#xA0;Gonbad Kavous, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hossein</FirstName>
        <LastName>Sanati</LastName>
        <affiliation locale="en_US">National&#xA0; Research Center for Genetic Engineering and Biotechnology, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zohreh</FirstName>
        <LastName>Jadali</LastName>
        <affiliation locale="en_US">Skin and Stem Cell Research Center, Tehran University of Medical Sciences, Tehran, Iran AND&#xA0;Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>12</Month>
        <Day>16</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>04</Month>
        <Day>04</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">T cells have been identified as key players in the pathogenesis of type 1 diabetes. However, the exact role of T-cell subpopulations in this pathway is presently unknown. The purpose of this study was to assess the expression pattern of two lineage-specifying transcription factors GATA-3 and T-bet, which are important in T helper type 1 (Th1) and Th2 cell development, respectively. Gene expression analysis of peripheral blood mononuclear cells (PBMCs) was performed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Plasma levels of IFN-&#x3B3; and IL-4 were also determined by ELISA. T-bet and IFN-&#x3B3; gene expression was significantly lower in patients group compared with healthy controls (p&lt;0.05). The expression of GATA-3 was relatively similar in patients and controls; however, IL-4 mRNAs were significantly increased in the PBMCs from patients as compared with normal controls (p&lt;0.05). In addition, a marked increase in plasma IL-4 levels were observed in patient group compared with controls (p&lt;0.001). To the contrary, IFN-&#x3B3; protein levels were decreased in patients in comparison with controls (p&lt;0.001). These data suggest additional implications of the role of Th1/Th2 imbalance for the immunopathogenesis of type 1 diabetes.

&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/734</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/734/655</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>15</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2016</Year>
        <Month>10</Month>
        <Day>31</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Association of New Putative Epitopes of Myelin Proteolipid Protein (58-74)  with Pathogenesis of Multiple Sclerosis</title>
    <FirstPage>394</FirstPage>
    <LastPage>402</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Zahra</FirstName>
        <LastName>Zamanzadeh</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB),&#xA0;Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ghasem</FirstName>
        <LastName>Ahangari</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB),&#xA0;Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mitra</FirstName>
        <LastName>Ataei</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB),&#xA0;Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Samie</FirstName>
        <LastName>Pouragahi</LastName>
        <affiliation locale="en_US">Qazvin University of Medical Sciences, Qazvin, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Seyed Massood</FirstName>
        <LastName>Nabavi</LastName>
        <affiliation locale="en_US">Department of Neurology , Shahed University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehdi</FirstName>
        <LastName>Sadeghi</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB),&#xA0;Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hossein</FirstName>
        <LastName>Sanati</LastName>
        <affiliation locale="en_US">Department of Medical Genetic, National Institute of Genetics Engineering and Biotechnology (NIGEB), Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>12</Month>
        <Day>08</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>04</Month>
        <Day>03</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Multiple sclerosis (MS) is an autoimmune disease in which auto-reactive T cells react with self-antigens expressed in the central nervous system (CNS). The main cause of MS is unknown. Nonetheless, the most probable theory is based on molecular mimicry, which suggests that some infections can activate T cells against brain auto-antigens like myelin proteolipid protein (PLP) and initiate the disease cascade. This study is conducted to evaluate the activatory effects of PLP58-74 on T lymphocytes and humoral immunity. PLP58-74 was considered as an immunodominant epitope candidate of PLP using bioinformatics tools. Patients and healthy individuals&#x2019; peripheral blood mononuclear cells (PBMCs) were treated with PLP58-74 and its proliferative effects were evaluated through assessing proliferating cell nuclear antigen (PCNA) gene expression changes by real time PCR and immunocytochemistry assay. Finally, the rate of CD4+ and CD8+ T cells were assessed by flowcytometry. ELISA was also performed to measure anti PLP58-74 antibody in patients&#x2019; serum. PLP58-74 induced proliferation in patients&#x2019; PBMCs while it did not influence PBMCs of healthy individuals. CD4+ T cells were the main activated cells in reaction to PLP58-74 which increased from 22% to 39.91%. In addition, immune assay showed threefold increase in specific anti PLP58-74 IgG in patients compared to healthy controls. Results showed that PLP58-74 can stimulate CD4+ T cells and humoral immunity. Therefore it seems that the epitopes of some microorganisms mimicking PLP such as PLP58-74 might have a potential role in the initiation of MS.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/725</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/725/777</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>15</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2016</Year>
        <Month>10</Month>
        <Day>31</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Enhanced Immune Responses against HIV-1 with Adenovector (Gag and Tat) Prime/Protein Boost Regimen and GM-CSF Injection</title>
    <FirstPage>403</FirstPage>
    <LastPage>412</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Negin</FirstName>
        <LastName>Hosseini Rouzbahani</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, Tarbiat Modares University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Saeed</FirstName>
        <LastName>Bayanolhagh</LastName>
        <affiliation locale="en_US">Iranian Research Center for HIV/AIDS, Iranian Institute for Reduction of High Risk Behaviors, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Gholami</LastName>
        <affiliation locale="en_US">Iranian Research Center for HIV/AIDS, Iranian Institute for Reduction of High Risk Behaviors, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ali</FirstName>
        <LastName>Esmaeilzadeh</LastName>
        <affiliation locale="en_US">Iranian Research Center for HIV/AIDS, Iranian Institute for Reduction of High Risk Behaviors, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zahra</FirstName>
        <LastName>Bayat Jozani</LastName>
        <affiliation locale="en_US">Iranian Research Center for HIV/AIDS, Iranian Institute for Reduction of High Risk Behaviors, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Minoo</FirstName>
        <LastName>Mohraz</LastName>
        <affiliation locale="en_US">Iranian Research Center for HIV/AIDS, Iranian Institute for Reduction of High Risk Behaviors, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ali Akbar</FirstName>
        <LastName>Pourfathollah</LastName>
        <affiliation locale="en_US">Department of Immunology, Faculty of Medicine, Tarbiat Modares University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>12</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>05</Month>
        <Day>28</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Vaccines against the HIV-1 virus offers the best hope for eliminating HIV-associated mortality. Recombinant adenovector type 5 (rAd5) vaccine is a potential candidate for preventive vaccine strategies. In this study, we evaluated the rAd5 prime/protein boost strategy in a murine model. We used rAd5 harboring single HIV-1 genes. These genes, including gag (p24) and exon1 of tat, were amplified from HIV-1 (clade A) RNA using nested PCR. Recombinant vectors were constructed, purified and then injected at 1012 viral particles into four groups, each comprising five mice. The groups were each assigned to receive one of rAd5 prime/protein boost Gag, Tat with and without recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF), and rAd5 with and without genes. The humoral responses were evaluated using ELISA and cellular immune responses checked by cell proliferation and ELISpot assays (IL-2, IL-4 and IFN-&#x3B3;). It was shown that compared with the rAd5 injection alone, the rAd5 prime/protein boost plan increased cellular immunity (p= 0.009) as well as humoral immunity (p= 0.009). Moreover, rGM-CSF as an adjuvant enhanced cell-mediated immunity and increased IL-4 expression (p=0.032). The results revealed that the simultaneous use of multiple antigens and heterologous prime/boost strategy can enhance both humoral and cellular immune systems. Moreover, subcutaneous injection of rGM-CSF increases IL-4 production and shifts the immune pattern to Th2. These strategies can potentially be used to develop an efficient HIV-1 vaccine.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/373</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/373/667</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>15</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2016</Year>
        <Month>10</Month>
        <Day>31</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Association between PTPN22/CTLA-4 Gene Polymorphism and  Allergic Rhinitis with Asthma in Children</title>
    <FirstPage>413</FirstPage>
    <LastPage>419</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Shang Hua</FirstName>
        <LastName>Song</LastName>
        <affiliation locale="en_US">Department of Otorhinolaryngology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China</affiliation>
      </Author>
      <Author>
        <FirstName>Xiao Qiang</FirstName>
        <LastName>Wang</LastName>
        <affiliation locale="en_US">Department of Otorhinolaryngology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China</affiliation>
      </Author>
      <Author>
        <FirstName>Yang</FirstName>
        <LastName>Shen</LastName>
        <affiliation locale="en_US">Department of Otorhinolaryngology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China</affiliation>
      </Author>
      <Author>
        <FirstName>Su Ling</FirstName>
        <LastName>Hong</LastName>
        <affiliation locale="en_US">Department of Otorhinolaryngology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China</affiliation>
      </Author>
      <Author>
        <FirstName>Xia</FirstName>
        <LastName>Ke</LastName>
        <affiliation locale="en_US">Department of Otorhinolaryngology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2016</Year>
        <Month>02</Month>
        <Day>27</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>05</Month>
        <Day>25</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Allergic rhinitis (AR) is an IgE-mediated upper airway disease, and its impact on asthma has been widely recognized. Protein tyrosine phosphatase non-receptor 22 (PTPN22) gene and the cytotoxic T-lymphocyte&#x2013;associated antigen 4 (CTLA-4) gene polymorphisms have been reported to be associated with several immune-related diseases. Here we investigated the reffect of these two genes&#x2019; polymorphisms on the risk of AR and asthma in Chinese Han children. A total of 106 AR patients, 112 AR with asthma patients, and 109 healthy children were enrolled in the study. The SNPs of PTPN22 (rs2488457, rs1310182, rs3789604) and CTLA-4 (rs3087243, rs11571302, rs11571315, rs231725, rs335219727, and rs4553808) were genotyped using a PCR-restriction fragment length polymorphism assay. For PTPN22, an increased prevalence of the CC genotype and C allele in rs1310182 were identified in AR group. For CTLA-4, AA genotype and A allele in rs3087243 and rs231725 were increased in AR with asthma group while in AR group, AA genotype and A allele in rs231725 were obviously decreased. This study reveals a significant association between SNPs in PTPN22, CTLA-4 gene and AR with asthma in Chinese Han children, which might be susceptibility factors for AR and asthma.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/826</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/826/671</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>15</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2016</Year>
        <Month>10</Month>
        <Day>31</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Identification of HLA Class I Misreads/Dropouts Using Serological Typing, in Comparison with DNA-based Typing</title>
    <FirstPage>420</FirstPage>
    <LastPage>425</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Hamid</FirstName>
        <LastName>Tipu</LastName>
        <affiliation locale="en_US">Department of Immunology, Armed Forces Institute of Pathology, Rawalpindi, Pakistan</affiliation>
      </Author>
      <Author>
        <FirstName>Muhammad</FirstName>
        <LastName>Bashir</LastName>
        <affiliation locale="en_US">Department of Immunology, Armed Forces Institute of Pathology, Rawalpindi, Pakistan</affiliation>
      </Author>
      <Author>
        <FirstName>Muhammad</FirstName>
        <LastName>Noman</LastName>
        <affiliation locale="en_US">Department of Immunology, Armed Forces Institute of Pathology, Rawalpindi, Pakistan</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2016</Year>
        <Month>01</Month>
        <Day>27</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2016</Year>
        <Month>05</Month>
        <Day>29</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Serology and DNA techniques are employed for Human Leukocyte Antigen (HLA) typing in different transplant centers. Results may not always correlate well and may need retyping with different technique. All the patients (with aplastic anemia, thalassemia, and immunodeficiency) and their donors, requiring HLA typing for bone marrow transplant were enrolled in the study. Serological HLA typing was done by complement-dependent lymphocytotoxicity while DNA-based typing was done with sequence specific primers (SSP). Serology identified 167 HLA A and 165 HLA B antigens while SSP in same samples iden