<?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>18</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>12</Month>
        <Day>04</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Hsp70 in Cancer: Partner or Traitor to Immune System</title>
    <FirstPage>589</FirstPage>
    <LastPage>604</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Mehdi</FirstName>
        <LastName>Vostakolaei</LastName>
        <affiliation locale="en_US">Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran AND Department of Pharmaceutical Biotechnology, Faculty of pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Jalal</FirstName>
        <LastName>Abdolalizadeh</LastName>
        <affiliation locale="en_US">Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran AND Paramedical Faculty, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Saeid</FirstName>
        <LastName>Hejazi</LastName>
        <affiliation locale="en_US">Department of Pharmaceutical Biotechnology, Faculty of pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran AND Department of Molecular Medicine, School of Advanced Biomedical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran AND Molecular Medicine Research Center, Biomedicine Institute, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Shirafkan</FirstName>
        <LastName>Kordi</LastName>
        <affiliation locale="en_US">Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ommoleila</FirstName>
        <LastName>Molavi</LastName>
        <affiliation locale="en_US">Department of Pharmaceutical Biotechnology, Faculty of pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran AND Biotechnology Research Center, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>08</Month>
        <Day>19</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>09</Month>
        <Day>14</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Heat shock protein 70.1 (Hsp70.1), also known as Hsp70, is a highly conserved member of the heat shock protein family that exists in all living organisms and determines the protein fate as molecular chaperones. Hsp70 basal expression is undetectable or low in most unstressed normal cells, however, its abundant presence in several types of human cancer cells is reported. Several studies support upregulated Hsp70 involved in tumor progression and drug resistance through modulation of cell death pathways and suppresses anticancer immune responses. However, numerous studies have confirmed that Hsp70 can also induce anticancer immune responses through the activation of immune cells in particular antigen-presenting cells (APCs). Regarding the significant and the promising role of vaccines in cancer immunotherapy, identification and characterization of the overexpressed Hsp70 as a potential immune stimulatory factor can pave the path for development of highly effective anticancer vaccines. In this review, we will discuss the interactions of Hsp70 with components of the immune system in cancers as well as possible strategies to harness Hsp70 for eliciting anticancer immune responses.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2493</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>30</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Relationship between Dietary Inflammatory Index, Pulmonary Functions and Asthma Control in Asthmatics</title>
    <FirstPage>605</FirstPage>
    <LastPage>614</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>&#xDC;m&#xFC;&#x15F;</FirstName>
        <LastName>&#xD6;zbey</LastName>
        <affiliation locale="en_US">Department of Nutrition and Diet, Health Science Faculty, Ankara University, Ankara, Turkey</affiliation>
      </Author>
      <Author>
        <FirstName>Asl&#x131;</FirstName>
        <LastName>U&#xE7;ar</LastName>
        <affiliation locale="en_US">Department of Nutrition and Diet, Health Science Faculty, Ankara University, Ankara, Turkey</affiliation>
      </Author>
      <Author>
        <FirstName>Nitin</FirstName>
        <LastName>Shivappa</LastName>
        <affiliation locale="en_US">Cancer Prevention and Control Program, University of South Carolina, Columbia, U.S.A AND Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, U.S.A</affiliation>
      </Author>
      <Author>
        <FirstName>James R</FirstName>
        <LastName>Hebert</LastName>
        <affiliation locale="en_US">Cancer Prevention and Control Program, University of South Carolina, Columbia, U.S.A AND Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, U.S.A</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>12</Month>
        <Day>06</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>06</Month>
        <Day>23</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">This cross-sectional study evaluates the relationship of the dietary inflammatory index (DII), a novel tool developed to measure the inflammatory capacity of a diet, with pulmonary functions and asthma control test (ACT) scores in asthmatic individuals. The study included 120 patients who were diagnosed with asthma for at least one year.&#xA0; The anthropometric measurements, one-day long nutrition uptake records, pulmonary function tests, and ACT scores of the respondents were recorded and compared according to categories of the DII which was calculated from 24- hour recalls. Forced vital capacity (FVC), forced expiratory volume in one second (FEV1) and ACT scores decreased with increasing DII tertiles (p&lt;0.05). The total energy, carbohydrate, fat, and saturated fat uptake of the participants increased in parallel to DII (p&lt;0.05); while vitamin A, C, and E uptakes, on the other hand, decreased as DII increased (p=0.0001). In conclusion, an increase in the inflammatory potential of diet among asthmatics decreases pulmonary functions and asthma control.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2215</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>16</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Value and Safety of High Flow Oxygenation in the Treatment of  Inpatient Asthma: A Randomized, Double-blind, Pilot Study</title>
    <FirstPage>615</FirstPage>
    <LastPage>623</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Sharare</FirstName>
        <LastName>Raeisi</LastName>
        <affiliation locale="en_US">Chronic Respiratory Diseases Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Atefeh</FirstName>
        <LastName>Fakharian</LastName>
        <affiliation locale="en_US">Chronic Respiratory Diseases Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Fariba</FirstName>
        <LastName>Ghorbani</LastName>
        <affiliation locale="en_US">Tracheal Diseases Research Center (TDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamid Reza</FirstName>
        <LastName>Jamaati</LastName>
        <affiliation locale="en_US">Chronic Respiratory Diseases Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam Sadaat</FirstName>
        <LastName>Mirenayat</LastName>
        <affiliation locale="en_US">Chronic Respiratory Diseases Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>12</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>06</Month>
        <Day>17</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">This study was aimed to compare the value and safety of high-flow nasal cannula (HFNC) and conventional oxygen therapy (COT) in patients with asthma exacerbation. In this randomized double-blind study, forthy patients with moderate-to-severe asthma exacerbations, aged 18 years or older were enrolled. Patients were randomly assigned to receive either HFNC or COT for 24 hours. Dyspnea scale, O2 saturation, spirometer indexes, respiratory and heart rate, and arterial blood gas (ABG) were compared within 2 and 24 hours of intervention. Dyspnea scale decreased significantly from 7.58&#xB1;1.04 to 6.45&#xB1;0.51 (p=0.000), and from 7.84&#xB1;1.7 to 6.89&#xB1;0.9 (p=0.049) within 2 hours in HFNC and COT groups, respectively. In the HFNC group, forced expiratory volume in one second (FEV1) was 1.48 &#xB1;0.94 L at the time of admission and increased to 1.61&#xB1;0.66 L (p=0.19) and 1.82&#xB1;0.92 L (p=0.003) after 2 and 24 hours of experience, respectively. In addition, in the COT group, FEV1 increased from 1.43&#xB1;0.65 L to 1.46&#xB1;0.53 L and 1.64&#xB1;0.6 L in the respective time-points, (p=0.071, 0.079). PaO2 and O2 saturation increased significantly in both groups during the first 2 hours. Two patients in the HFNC group had the complaint of nasal irritation and the device-produced heat; while one patient in the COT group needed more respiratory care. HFNC could be a therapeutic option for asthma exacerbation among adult patients after considering the patient&#x2019;s selection.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2306</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>12</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Rosuvastatin Affects Tracheal Responsiveness, Bronchoalveolar  Lavage Inflammatory Cells, and Oxidative Stress Markers in Hyperlipidemic and Asthmatic Rats</title>
    <FirstPage>624</FirstPage>
    <LastPage>638</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Saeideh</FirstName>
        <LastName>Saadat</LastName>
        <affiliation locale="en_US">Department of Physiology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran AND&#xA0;&#xA0;Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Amin</FirstName>
        <LastName>Mokhtari-Zaer</LastName>
        <affiliation locale="en_US">Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran AND Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mousa-Al-Reza</FirstName>
        <LastName>Hadjzadeh</LastName>
        <affiliation locale="en_US">Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran AND Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hossein</FirstName>
        <LastName>Boskabady</LastName>
        <affiliation locale="en_US">Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran AND Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>04</Month>
        <Day>19</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>05</Month>
        <Day>25</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Statins provide greater protection than predicted from just cholesterol-lowering effects, which is possibly mediated by other pleiotropic actions. This study aimed to examine the possible interaction effect of asthma on lipid profiles and evaluate the effect of rosuvastatin treatment on asthma. The animals were assigned into (1) control, (2) asthmatic, (3) hyperlipidemic, (4) asthmatic-hyperlipidemic, (5) rosuvastatin (40 mg/kg/day intraperitoneally, for 3 weeks)-treated asthmatic, (6) rosuvastatin-treated hyperlipidemic and (7) rosuvastatin-treated asthmatic-hyperlipidemic groups. Tracheal responsiveness to methacholine and ovalbumin, total and differential WBC (white blood cell) counts, and oxidative stress markers in bronchoalveolar lavage fluid (BALF) were evaluated. In the asthmatic and asthmatic-hyperlipidemic groups, tracheal responsiveness to ovalbumin, total WBC count, numbers of eosinophils, neutrophils, and monocytes were higher than the control group (p&lt;0.001). A left-ward shift in the concentration-response curves to methacholine, an increase in nitrite and malondialdehyde concentrations, and a decrease in total thiol content, superoxide dismutase and catalase activities were also observed in the asthmatic and asthmatic-hyperlipidemic groups compared to control group (p&lt;0.01 to p&lt;0.001). Beyond lipid-lowering effect in the treated hyperlipidemic and asthmatic-hyperlipidemic groups, rosuvastatin treatment decreased tracheal responsiveness to methacholine, reduced total WBC count, the numbers of eosinophils, neutrophils, and monocytes, as well as decreased malondialdehyde concentration, and increased total thiol content, superoxide dismutase and catalase activities in treated asthmatic and asthmatic-hyperlipidemic groups (p&lt;0.05 to p&lt;0.001). The improving effect of rosuvastatin on asthmatic and asthmatic-hyperlipidemic animals was shown due to pleiotropic mechanisms including the effect on airway hyperresponsiveness, lung inflammation, and oxidative stress.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2367</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>11</Month>
        <Day>11</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Effect of Guluronic Acid (G2013), As a New Anti-inflammatory Drug on Gene Expression of Pro-inflammatory and Anti-inflammatory Cytokines and Their Transcription Factors in Rheumatoid Arthritis Patients</title>
    <FirstPage>639</FirstPage>
    <LastPage>648</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Tahereh</FirstName>
        <LastName>Bakhtiari</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>ShahinKhadem</FirstName>
        <LastName>Azarian</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Afshin</FirstName>
        <LastName>Ghaderi</LastName>
        <affiliation locale="en_US">Department of Internal Medicine, Hematology and Medical Oncology Ward, Cancer Research Centre,  Cancer Institute, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Arman</FirstName>
        <LastName>Ahmadzadeh</LastName>
        <affiliation locale="en_US">Department of Rheumatology, Loghman Hakim Hospital, Shahid Beheshti 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, Tehran University of Medical Sciences, Tehran, Iran AND Research Center for Immunodeficiencies, Children's Medical Centre, Tehran University of Medical  Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>05</Month>
        <Day>26</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>07</Month>
        <Day>10</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Rheumatoid arthritis (RA) as a long-term autoimmune disease is characterized by pain, swelling and joints destruction. The therapeutic efficacy of Guluronic acid (G2013) (patented, DEU: 102016113017.6) was reported in phase I/II clinical trial in RA patients. In this study, we aimed to evaluate the effect of G2013 as a novel non-steroidal anti-inflammatory drug (NSAID) with immunosuppressive property on genes expression of anti-inflammatory and pro-inflammatory cytokines and their transcription factors in the blood sample of RA patients. This study was performed on 12 patients with RA who had an inadequate response to conventional treatments which were disease-modifying anti-rheumatic drugs (DMARDs), NSAID, and biologics. G2013 was administered orally at a dose of 500 mg twice daily for 12 weeks. Before and after the treatment of patients with drug G2013, the peripheral blood mononuclear cells (PBMCs) were isolated for evaluating the gene expression level of interleukin 10 (IL10), interleukin 22 (IL22), interferon &#x3B3; (IFN&#x3B3;), and transcription factors specific to the T helper cell lineages, forkhead box P3 (Fox-P3), Aryl hydrocarbon receptor (AHR) and T-box&#x2013;containing protein expressed in T cells (T-bet) using the real-time PCR method. Since these cytokines have a key role in the progression of RA and disease condition expected induction of IFN&#x3B3;, AHR, IL22, T-bet, and reduction of IL10, Fox-P3. Results indicated a significant reduction in the level of IFN&#x3B3;, AHR and a significant induction in IL10, Fox-P3 gene expression in comparison with the control group. In conclusion; the results of this investigation showed a part of the immunological mechanism of G2013 as a novel anti-inflammatory that could reduce pro-inflammatory cytokine and their transcription factors. Furthermore, it increased the anti-inflammatory cytokine and its transcription factor (clinical trial identifier: IRCT2016092813739N5).</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2418</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>11</Month>
        <Day>27</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">A Randomized Control Trial Study to Determine the Effect of Melatonin on Serum Levels of IL-1&#x3B2; and TNF-&#x3B1; in Patients with Multiple Sclerosis</title>
    <FirstPage>649</FirstPage>
    <LastPage>654</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Masoomeh</FirstName>
        <LastName>Yosefifard</LastName>
        <affiliation locale="en_US">Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Gholamhassan</FirstName>
        <LastName>Vaezi</LastName>
        <affiliation locale="en_US">Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ali Akbar</FirstName>
        <LastName>Malekirad</LastName>
        <affiliation locale="en_US">Department of Biology, Payame Noor University, Tehran, Iran AND Toxicology and Diseases Group, Pharmaceutical Science Research Center, Tehran University of  Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Fardin</FirstName>
        <LastName>Faraji</LastName>
        <affiliation locale="en_US">Department of Neurology, School of Medicine, Arak University of Medical Sciences, Arak, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Vida</FirstName>
        <LastName>Hojati</LastName>
        <affiliation locale="en_US">Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>04</Month>
        <Day>09</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>05</Month>
        <Day>20</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Multiple sclerosis (MS) is the most common neurological disease that happens at a young age. MS is an inflammatory disease; associated with the demyelination of the central nervous system. Therefore, some inflammatory factors are effective in the mechanism and progression of the disease. Melatonin, as a multi-effect substance including anti-inflammatory effects, can reduce symptoms of MS in patients with a change in their inflammatory factors level. In this study, 50 MS patients who were referred to the MS Society of Markazi Province were randomly selected. All patients were treated with routine MS treatment (interferon) and were divided into control (25 placebo recipients) and treatment (25 recipients of 3 mg melatonin per day for 24 weeks) groups. Anthropometric data of patients including height, weight, and age were determined. Blood samples were collected after fasting in order to determine serum levels of interleukin 1 beta (IL-1&#x3B2;) and tumor necrosis factor-alpha&#xA0;(TNF-&#x3B1;). Then, samples were immediately centrb_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>18</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>23</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Immunological Responses against HER2-targeted Idarubicin-ZHER2 Conjugate in BALB/c Mice</title>
    <FirstPage>501</FirstPage>
    <LastPage>510</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Leila</FirstName>
        <LastName>Siavoshinia</LastName>
        <affiliation locale="en_US">Department of Biochemistry, Faculty of Medicine, Ahvaz Jundishapur  University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mostafa</FirstName>
        <LastName>Jamalan</LastName>
        <affiliation locale="en_US">Abadan Faculty of Medical Sciences, Abadan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Majid</FirstName>
        <LastName>Zeinali</LastName>
        <affiliation locale="en_US">Biotechnology Research Center, Research Institute of Petroleum Industry (RIPI), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ghorban</FirstName>
        <LastName>Mohammadzadeh</LastName>
        <affiliation locale="en_US">Department of Clinical Biochemistry, Hyperlipidemia Research Center, Faculty of Medicine,  Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>07</Month>
        <Day>28</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>05</Month>
        <Day>11</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Targeting of cancerous cells with a high level of human epidermal growth factor receptor 2 (HER2) expressions by drug immunoconjugates is a new approach for specific delivery of chemotherapeutic agents. Our previous work indicated that idarubicin-ZHER2 affibody conjugate has a great potential for the treatment of HER2-overexpressing malignant cell lines but possible induced immune response against constructed conjugate was not addressed. In the current study, the possibility of induction of humoral and cellular immune responses against idarubicin-ZHER2 affibody conjugate in BALB/c mice was investigated. For assessment of the induced immune response, prepared and qualified idarubicin-ZHER2 affibody conjugate was administrated intravenously to BALB/c mice and the induced cellular immune response was evaluated by measuring secretion levels of interferon gamma (IFN-&#x3B3;) and interleukin 10 (IL-10) cytokines by the splenocytes. Humoral response of treated mice was also assessed by measuring total immunoglobulin G (IgG) titer in mice sera. The obtained results showed that idarubicin-ZHER2 affibody conjugate at any examined concentrations could not induce secretion of IFN-&#x3B3; as a pro-inflammatory cytokine. A mild increase in the level of regulatory IL-10 cytokine was seen in the treated mice although no dose dependency in the level of IL-10 production was observed. Furthermore, results showed that idarubicin-ZHER2 conjugate could not induce IgG production in the treated mice. Based on these findings, the idarubicin-ZHER2 conjugate can be considered as a candidate for the development of new therapeutics against HER2-overexpressing cancers although further in vivo studies are needed.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2075</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>23</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Immunogenicity Evaluation of Recombinant Edible Vaccine Candidate Containing HER2-MUC1 against Breast Cancer</title>
    <FirstPage>511</FirstPage>
    <LastPage>522</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Mahdieh</FirstName>
        <LastName>Mehrab Mohseni</LastName>
        <affiliation locale="en_US">Department of Agricultural Biotechnology, National Institute for Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Jafar</FirstName>
        <LastName>Amani</LastName>
        <affiliation locale="en_US">Applied Microbiology Research Center, Systems Biology and Poisonings Institute,  Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahdi</FirstName>
        <LastName>Fasihi Ramandi</LastName>
        <affiliation locale="en_US">Molecular Biology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Forouzandeh</FirstName>
        <LastName>Mahjoubi</LastName>
        <affiliation locale="en_US">Department of Medical Biotechnology, National Institute for Genetic Engineering  and Biotechnology (NIGEB), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahyat</FirstName>
        <LastName>Jafaria</LastName>
        <affiliation locale="en_US">Department of Agricultural Biotechnology, National Institute for Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ali Hatef</FirstName>
        <LastName>Salmanian</LastName>
        <affiliation locale="en_US">Department of Agricultural Biotechnology, National Institute for Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>12</Month>
        <Day>18</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>05</Month>
        <Day>26</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Human epithelial growth factor receptor2 (Her2) and polymorphic epithelial mucin (MUC1) are tumor-associated antigens that have been extensively investigated in adenocarcinomas. Generally, each of these molecules was used separately for diagnosis of adenocarcinomas and as an injective vaccines in cancer therapy researches, but not in the chimeric form as an edible immunogen. In this study, Her2, MUC1, and a novel fusion structure were expressed in the seeds and hairy roots of transgenic plants appropriately. The mice groups were immunized either by feeding of transgenic seeds or hairy roots.&#xA0;All immunized groups showed a considerable rise in anti-glycoprotein serum IgG and IgA, and IFN&#x263; cytokine. However, the animals received chimeric protein showed significant higher immune responses in comparison to ones received one of these immunogen. The results indicated that the oral immunization of an animal model with transgenic plants could effectively elicit immune responses against two major tumor-associated antigens.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2237</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>23</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Effect of Aqueous Extract of Tarragon on Clinical Symptoms and T Cell Differentiation in Experimental Autoimmune Encephalomyelitis</title>
    <FirstPage>523</FirstPage>
    <LastPage>532</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Tayebeh</FirstName>
        <LastName>Nowras</LastName>
        <affiliation locale="en_US">Student Research Committee, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Fereidouni</LastName>
        <affiliation locale="en_US">Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamidreza</FirstName>
        <LastName>Safari</LastName>
        <affiliation locale="en_US">Student Research Committee, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohsen</FirstName>
        <LastName>Naseri</LastName>
        <affiliation locale="en_US">Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>10</Month>
        <Day>28</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>05</Month>
        <Day>22</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Multiple sclerosis (MS) is one of the autoimmune diseases that affects the central nervous system (CNS) and causes myelin loss and axonal damage. Recent studies have shown the important role of autoreactive T cells in the pathogenesis of MS. One of the plants in the Astersa family, which has therapeutic benefits is Artemisia dracunculus L. or Tarragon. In this study, the role of aqueous extract of Tarragon in suppressing Th1 and Th17 cell differentiation and ameliorating experimental autoimmune encephalomyelitis (EAE) was investigated. EAE was induced in C57BL/6 female mice by Hook kit MOG35-55/CFA Emulsion PTX and one group was treated with Tarragon at a dose of 500 mg/kg. Mice were euthanized on day 33 post-immunization, spleens were removed for assessing Th1, Th17 and Treg cells by flow cytometry. We provided evidence that Tarragon (500 mg/kg) significantly ameliorated clinical scores of EAE. We did not observe significant alterations in T cell differentiation to Th1, Th17 or Treg in the spleen of mice during EAE. This is the first experimental evidence showing that administration of aqueous extract of Tarragon reduces the severity of EAE, but the protective effect of Tarragon is independent of alteration in T cells in the spleen. These results suggest other mechanisms for the effectiveness of this extract in improving the EAE process.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2177</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>23</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Synergistic Effect of Fluvastatin and IFN-&#x3BB; on Peripheral Blood Mononuclear Cells of Chronic Hepatitis C Virus (HCV) Patients with IL-28B rs12979860 CC Genotype</title>
    <FirstPage>533</FirstPage>
    <LastPage>542</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Amin</FirstName>
        <LastName>Farzanegan Gharabolagh</LastName>
        <affiliation locale="en_US">Department of Virology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Taravat</FirstName>
        <LastName>Bamdad</LastName>
        <affiliation locale="en_US">Department of Virology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehdi</FirstName>
        <LastName>Hedayati</LastName>
        <affiliation locale="en_US">Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Seyed Ali</FirstName>
        <LastName>Dehghan Manshadi</LastName>
        <affiliation locale="en_US">Department of Infectious Diseases and Tropical Medicine, Imam Khomeini Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>09</Month>
        <Day>14</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
        <Month>11</Month>
        <Day>04</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">There is a relationship between the life cycle of the hepatitis C virus (HCV) and the synthesis and hemostasis of lipids as well as lipid metabolism and interferon (IFN) regulatory system. This study was aimed to examine the effect of fluvastatin and IFN-&#x19B; in the expression of mediators involved in lipid metabolism and HCV proliferation in patients with rs12979860 CC polymorphism. Thirteen patients with HCV and five controls with rs1297986CC polymorphism were included in this study. Peripheral blood mononuclear cells (PBMCs) of patients and controls were treated by fluvastatin, IFN-&#x3BB; or fluvastatin+IFN-&#x3BB;. Assessment of IL-28B polymorphism, RNA extraction, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was performed. The mRNA expression of sterol regulatory element-binding protein 1 c (SREBP1c), ATP-binding cassette transporter A1 (ABCA1), diacylglycerol acyltransferase 1 (DGAT1), and HCV core as well as measurement of ABCA1 protein level were evaluated before and after treatment. The results indicated that IFN-&#x3BB; +fluvastatin acted as an inhibitor in mRNA expression of SREBP1c; while acting as an inducer in the expression of ABCA-1. The results of ABCA1 assay showed a significant increase of this protein after treatment with fluvastatin and IFN-&#x3BB; compared with untreated cells (p=0.02). Moreover, the mRNA expression of HCV core was suppressed in all experimental groups treated with fluvastatin, IFN-&#x3BB; or their combination which was more significant after treatment with fluvastatin+IFN-&#x3BB; (p&lt;0.001). The results of this study demonstrated the significant effect of treatment with fluvastatin+IFN-&#x3BB; in PBMCs of HCV patients with rs12979860 CC polymorphism. According to the drug resistance of viruses and prevention of virus-induced steatosis in patients with HCV, using regulatory agents of lipid mediators in parallel with current medications could be considered as an effective therapeutic strategy.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2150</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>23</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Anti-varicella Zoster Virus IgG and hsCRP Levels Correlate with Progression of Coronary Artery Atherosclerosis</title>
    <FirstPage>543</FirstPage>
    <LastPage>553</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Hamed</FirstName>
        <LastName>Fouladseresht</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Atefe</FirstName>
        <LastName>Ghamar Talepoor</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Shirin</FirstName>
        <LastName>Farjadian</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Shahdad</FirstName>
        <LastName>Khosropanah</LastName>
        <affiliation locale="en_US">Department of Cardiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mehrnoosh</FirstName>
        <LastName>Doroudchi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>06</Month>
        <Day>12</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>07</Month>
        <Day>17</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">The relationship between high levels of anti-Varicella Zoster Virus (VZV) IgG in cerebrospinal fluid (CSF) and cerebrovascular atherosclerosis commends a possible similar association in other vessels. We aimed to investigate the association of VZV-seropositivity with coronary artery atherosclerosis. We recruited 88 newly diagnosed patients with more than 50% stenosis in at least one of the main coronary arteries. As the control group, 99 age-matched individuals with normal/insignificant coronary artery findings were included. Clinical, paraclinical, and demographical data were gathered at the time of sampling. High&#x2010;sensitivity C&#x2010;reactive protein (hsCRP) levels were measured by nephelometry. VZV-seropositivity was determined by measuring of anti-VZV IgG level in plasma. Multivariable logistic regression was used to evaluate the correlation of data with coronary vascular atherosclerosis. The frequency of VZV-seropositivity was significantly higher in the atherosclerosis group compared to the controls (OR=1.88; 95%CI=1.03-3.44). The plasma levels of anti-VZV IgG were significantly higher in patients with atherosclerosis (Median=2.70, IQR=1.53-4.30 AU/mL) than in the controls (Median=2.10, IQR=1.70-3.10 AU/mL, p=0.034). The hsCRP levels in patients and controls were 5.19&#xB1;2.00 and 1.51&#xB1;1.07 mg/L, respectively. The correlation between hsCRP and anti-VZV IgG level in plasma was observed (r=0.40, p&lt;0.001). The levels of hsCRP and anti-VZV IgG increased based on the number of diseased vessels but only the difference in hsCRP levels reached a significant level (p&lt;0.001 and p=0.168, respectively). Our data suggest that VZV-seropositivity and hsCRP elevation jointly increase the risk of atherosclerosis. The multifactorial nature of atherosclerosis; however, leaves more options for the inflammatory milieu to be generated.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2436</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>23</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Immune Modulatory Effects of Hypercholesterolemia:  Can Atorvastatin Convert the Detrimental Effect of Hypercholesterolemia  on the Immune System?</title>
    <FirstPage>554</FirstPage>
    <LastPage>566</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Zeinab</FirstName>
        <LastName>Emruzi</LastName>
        <affiliation locale="en_US">Department of Medical Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Pegah</FirstName>
        <LastName>Babaheidarian</LastName>
        <affiliation locale="en_US">Department of Pathology, Rasul-e Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahmoud</FirstName>
        <LastName>Arshad</LastName>
        <affiliation locale="en_US">Department of Internal Medicine and Endocrinology, Minimally Invasive Surgery Research Center,  Rasul-e Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hannes</FirstName>
        <LastName>Stockinger</LastName>
        <affiliation locale="en_US">Institute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Molecular Immunology Unit, Vienna, Austria</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), Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>07</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>05</Month>
        <Day>04</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Many observations showed that hypercholesterolemia can disrupt immune response. Statin drugs that were used for the treatment of hypercholesterolemia patients can interfere in the regulation of the immune response and cytokine secretion. The primary aim of the current study was to investigate the immune response among treatment-na&#xEF;ve patients with hypercholesterolemia and healthy subjects. The secondary goal of the study was to determine whether atorvastatin can reverse the detrimental effect of hypercholesterolemia on the immune system. Peripheral blood mononuclear cells (PBMCs) were isolated from 50 patients afflicted with hypercholesterolemia who were treatment-na&#xEF;ve along with 50 sex/age-matched hypercholesterolemia patients receiving atorvastatin, and 50 sex/age-matched healthy subjects. Quantitative PCR and ELISA methods were used for gene and protein expression analysis of T helper 1 (Th1) and Th2 related cytokines. Additionally, the expression of the cluster of differentiation (CD) markers on T, B, and natural killer (NK) cells was measured by flow cytometry method. The results showed that hypercholesterolemia and atorvastatin down-regulated the expression of Th1-related cytokines and elevated the levels of Th2-related cytokines. The expression of cell surface markers, CD25 and CD69, was significantly decreased in the treatment-na&#xEF;ve, and atorvastatin groups. It seems that atorvastatin is not able to repair the deleterious effects of hypercholesterolemia on the immune system. Moreover, elevated levels of cholesterol along with the administration of atorvastatin tilt the Th1/Th2 balance in favor of Th2 and reduce T cell activation.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2302</web_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Allergy, Asthma and Immunology</JournalTitle>
      <Issn>1735-1502</Issn>
      <Volume>18</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>23</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Antiepileptic Hypersensitivity Syndrome to Phenobarbital:  A Case Report</title>
    <FirstPage>567</FirstPage>
    <LastPage>571</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Zahra</FirstName>
        <LastName>Nafei</LastName>
        <affiliation locale="en_US">Children Growth Disorders Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nasrin</FirstName>
        <LastName>Behniafard</LastName>
        <affiliation locale="en_US">Department of Allergy and Immunology, Shahid Sadoughi University of Medical Sciences, Yazd, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Farzane</FirstName>
        <LastName>Shefai</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Shahid Sadoughi University of Medical Sciences, Yazd, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>06</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>05</Month>
        <Day>20</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Phenobarbital is still one of the most commonly used medical treatments for different types of seizures. It has numerous different side-effects. Antiepileptic hypersensitivity syndrome (AHS) is a rare and potentially life-threatening adverse reaction to aromatic anticonvulsants such as phenobarbital. Its characteristic features are fever, rash, and lymphadenopathy with different severity of hematologic abnormalities. This case report presents a 26-month-old girl that developed fever, disseminated maculopapular rash, petechiae and thrombocytopenia two weeks after the initiation of phenobarbital prescribed for febrile seizure prophylaxis. The patient was admitted in our center with the impression of hypersensitivity syndrome, so phenobarbital was discontinued and her treatment was resumed with methylprednisolone and intravenous immunoglobulin. After a few days, all symptoms improved and the platelet count was normalized. Thrombocytopenia is a rare complication of hypersensitivity syndrome to phenobarbital in children. Paying attention to this point can pr