<?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 centrd using ELISA. The expression levels of the transcriptional and translational factors in the lungs were examined using Quantitative Reverse Transcriptase Polymerase Chain reaction (qRT-PCR) and western blot. The expression levels of leptin in the BALF of normal weight group, asthma group, obese group and obese asthma group were 2.032&#xB1;0.133, 5.375&#xB1;0.123, 5.418&#xB1;0.165 and 7.486&#xB1;0.168, respectively. The expression of leptin in obese asthma group was the highest (p&lt;0.05) &#xFF0C;while the expression of adiponectin the lowest (p&lt;0.05). The expression level of P-STAT3 in the obese asthma group was 0.9244&#xB1;0.014, and was significantly higher than three other groups (p&lt;0.05). The expressions of P-STAT6 in three other groups were all significantly higher than normal weight group (p&lt;0.05). Our data suggest that the function of leptin on the pulmonary inflammation of obese asthma may be partly through activating the STAT3 signaling pathway.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1739</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1739/1387</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>18</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Increase of pFAK and THBS1 Protein and Gene Expression Levels in Vascular Smooth Muscle Cells by Histamine-treated M1 Macrophages</title>
    <FirstPage>72</FirstPage>
    <LastPage>79</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Mohsen</FirstName>
        <LastName>Khosravi</LastName>
        <affiliation locale="en_US">Department of Biochemistry, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Najafi</LastName>
        <affiliation locale="en_US">Department of Biochemistry, Iran University of Medical Sciences, Tehran, Iran AND Molecular and Cellular Research Center, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abdollah</FirstName>
        <LastName>Amirfarhangi</LastName>
        <affiliation locale="en_US">Department of Cardiology, Hazrat Rasool Akrsm Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahdi</FirstName>
        <LastName>Karimi</LastName>
        <affiliation locale="en_US">Department of Medical Nanotechnology, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Fahimeh</FirstName>
        <LastName>Fattahi</LastName>
        <affiliation locale="en_US">Oncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran AND&#xA0;Department of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Shabani</LastName>
        <affiliation locale="en_US">Department of Biochemistry, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>05</Month>
        <Day>01</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
        <Month>07</Month>
        <Day>03</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Atherosclerosis is developed due to the formation of atheroma plaques in the coronary arteries. In this process, M1 macrophages and vascular smooth muscle cells (VSMCs) are the main functional cells. Inflammatory mediators such as histamine may inflame M1 macrophages. The aim of this study was to determine the effect of M1 macrophage secretion contents on the gene and protein expression levels of focal adhesion kinase (FAK), vasodilator-stimulated phosphoprotein (VASP), and thrombospondin1 (THBS1). Whole blood samples from the six healthy subjects (stenosis&lt;5%), and six patients (stenosis&gt;70%) were prepared and peripheral blood mononuclear cells (PBMCs) were isolated. Then monocytes were differentiated into M1 macrophages using 100 ng/mL granulocyte-macrophage colony stimulating factor (GM-CSF). The differentiated M1 macrophages were treated with histamine (10-6 M), and their secretion contents were harvested and added to the culture medium of VSMCs. The FAK, VASP, and THBS1 gene expression and protein levels were measured using RT-qPCR and western blot techniques in VSMCs, respectively. The FAK and THBS1 gene expression levels significantly increased in VSMCs after adding secretion contents obtained from histamine-treated M1 macrophages (p=0.023 and 0.05, respectively), while significant results were not observed for VASP gene (p=0.45). In converse with the phosphorylated VASP (pVASP) (p&lt;0.34), the phosphorylated FAK (pFAK) and THBS1 protein levels increased in VSMCs (p&lt;0.001). We concluded that in inflammatory conditions, the immune events could affect the macrophages by histamine. The activated macrophages could locally activate signaling pathways via FAK and THBS1 genes that are effective in the proliferation and migration of VSMCs.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1943</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1943/1393</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>18</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Anti-tumoral Effect of &#x3B2;-D-Mannuronic Acid (M2000) as a Novel NSAID on Treg Cells Frequency and MMP-2, MMP-9, CCL22 and TGF&#x3B2;1 Gene Expression in Pre-surgical Breast Cancer Patients</title>
    <FirstPage>80</FirstPage>
    <LastPage>90</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Sarvenaz</FirstName>
        <LastName>Kashefi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hamid</FirstName>
        <LastName>Ahmadi</LastName>
        <affiliation locale="en_US">Breast Disease Research Center (BDRC), Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ramesh</FirstName>
        <LastName>Omranipour</LastName>
        <affiliation locale="en_US">Breast Disease Research Center (BDRC), Tehran University of Medical Sciences, Tehran, Iran  AND Department of Surgical Oncology, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Habibollah</FirstName>
        <LastName>Mahmoodzadeh</LastName>
        <affiliation locale="en_US">Department of Surgical Oncology, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Fahimeh</FirstName>
        <LastName>Jafarnezhad-Ansariha</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Farzaneh</FirstName>
        <LastName>Tofighi Zavareh</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran AND Department of Surgical Oncology, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abbas</FirstName>
        <LastName>Mirshafiey</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran AND Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of  Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>09</Month>
        <Day>28</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
        <Month>12</Month>
        <Day>03</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">With respect to the role of chronic inflammation in the induction and progression of breast cancer (BC). The relationship between tumor and tumor microenvironment may be a hopeful strategy for BC therapy. According to the effect of &#x3B2;-D-Mannuronic acid (M2000) as a novel non-steroidal anti-inflammatory drug (NSAID) on BC murine model and 4T1 cell line, we started to study that was a phase II, randomized, controlled clinical trial. 24 women with BC were included in this study and were followed by fixed oral doses of M2000, 500 mg two times a day (6-8 weeks). Blood samples were collected at baseline and weeks 6-8. To compare the patterns of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), C-C motif chemokine ligand 22 (CCL22) and The transforming growth factor-beta 1 (TGF&#x3B2;1) gene expression and T regulatory cells (Tregs) frequency of healthy women normal controls with BC patients, a set of 10 blood samples of&#xA0; women healthy volunteers was collected. The gene expression was evaluated by quantitative Real-time PCR (qRT-PCR) and the frequency of Tregs was assessed by flow cytometry. Our results showed, reduction in MMP-2 (p=0.08), MMP-9 (p=0.03), CCL22 (p=0.003) and TGF&#x3B2;1 (p=0.1) gene expression and Tregs frequency (p=0.01) which play a main role in the development of chronic inflammation, angiogenesis, tumorigenesis and metastasis. Our findings demonstrated that M2000 therapy as a novel designed NSAID had valuable therapeutic effects on BC. No adverse effects were observed following the use of M2000 after 6-8 weeks.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2157</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/2157/1401</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>18</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Association between Interleukin-32 and Interleukin-17A Single Nucleotide Polymorphisms and Serum Levels with Polycystic Ovary Syndrome</title>
    <FirstPage>91</FirstPage>
    <LastPage>99</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Fateme</FirstName>
        <LastName>Hesampour</LastName>
        <affiliation locale="en_US">Department of Immunology, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Bahia</FirstName>
        <LastName>Namavar Jahromi</LastName>
        <affiliation locale="en_US">Infertility Research Center, Shiraz University of Medical Sciences, Shiraz, Iran AND Department of Gynecology and Obstetrics, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Foroozan</FirstName>
        <LastName>Tahmasebi</LastName>
        <affiliation locale="en_US">Department of Immunology, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Behrouz</FirstName>
        <LastName>Gharesi-Fard</LastName>
        <affiliation locale="en_US">Department of Immunology, Shiraz University of Medical Sciences, Shiraz, Iran AND Infertility Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>10</Month>
        <Day>31</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
        <Month>12</Month>
        <Day>29</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Polycystic ovary syndrome (PCOS) is correlated with low-grade chronic inflammation. Interleukin-17A (IL-17A) and Interleukin-32 (IL-32) are two members of the pro-inflammatory cytokines which act as significant components of the immune system during certain inflammatory diseases. Along with immunological processes, genetic factors play major roles in predisposition to PCOS. There are myriad single nucleotide polymorphisms (SNPs) within IL-17A and IL-32 genes that may affect their production and the susceptibility of individuals to PCOS. The objective of the present research was to investigate the association between IL-17A (rs2275913) and IL-32 (rs9927163, rs4786370) SNPs, and also their serum levels with susceptibility to PCOS in a group of Iranian women. In this case-control study, 150 PCOS patients (mean age of 29.1 years) and 150 healthy women (mean age of 26.1 years) were analyzed in terms of IL-17A and IL-32 SNPs via polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Furthermore, serum levels of IL-17A and IL-32 cytokines were measured through the use of ELISA method. There were significant differences between PCOS and healthy women regarding IL-17A rs2275913 alleles, genotypes frequencies (p=0.005, and 0.01, respectively) and the allelic distribution of IL-32 rs9927163 SNP (p=0.03). Additionally, significant differences were indicated between two groups concerning the AG genotype against AA+GG genotypes (p=0.009) and the GG genotype against AA+AG genotypes (p=0.006) in IL-17A rs2275913 SNP. In the matter of IL-32 gene SNPs, GC haplotype frequency was significantly different between patients and controls (p=0.05). Furthermore, IL-32 serum level was not significantly different between the two studied groups and the serum level of IL-17A was not detectable. In conclusion, IL-17A and IL-32 SNPs might be associated with predisposition to PCOS in Iranian women.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2180</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/2180/1397</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>18</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Role of Progesterone in Cellular Apoptosis of Skin and Lung in a Bleomycin-injured Mouse Model</title>
    <FirstPage>100</FirstPage>
    <LastPage>107</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Fatemeh</FirstName>
        <LastName>Vafashoar</LastName>
        <affiliation locale="en_US">Department of Immunology, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hadi</FirstName>
        <LastName>Poormoghim</LastName>
        <affiliation locale="en_US">Scleroderma Study Group, Firoozgar Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Kazem</FirstName>
        <LastName>Mousavizadeh</LastName>
        <affiliation locale="en_US">Department of Molecular Medicine, Faculty of Advanced Technologies in Medicine,  Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Tahereh</FirstName>
        <LastName>Mousavi Shabestari</LastName>
        <affiliation locale="en_US">Institute of Immunology and Infectious Disease, Antimicrobial Resistance Research Center, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abbas</FirstName>
        <LastName>Tavasoli</LastName>
        <affiliation locale="en_US">Department of Pathobiology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Seyed Ali</FirstName>
        <LastName>Javadmoosavi</LastName>
        <affiliation locale="en_US">Air Pollution Research Centre, School of Public Health, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nazanin</FirstName>
        <LastName>Mojtabavi</LastName>
        <affiliation locale="en_US">Department of Immunology, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>02</Month>
        <Day>04</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
        <Month>06</Month>
        <Day>18</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Systemic sclerosis is a female predominant, a fibrotic autoimmune disease in which disturbance in tissue homeostasis and cell turnover including cell apoptosis are central events in pathogenesis. Sex hormones are known as the important players in sexual dimorphism of autoimmune diseases and in tissue homeostasis. Progesterone influences autoimmune disease via its immunomodulatory effect or by its direct action on parenchymal cell function. On the other hand, this hormone impacts tissue homeostasis by acting on cell apoptosis in a different situation. The objective of this study was to examine the effect of progesterone on cellular apoptosis of skin and lung tissues in a mouse model of scleroderma. Four group of mice were involved in this study with 10 mice in each. The fibrotic model was induced by daily subcutaneous injection of bleomycin for 28 days. One week after initiation of fibrosis induction, mice received subcutaneous progesterone alone or with bleomycin for 21 days. Control group received only Phosphate buffered saline PBS. After 28 days, under lethal anesthesia skin and lung tissues were harvested for histological assessment and hydroxyproline measurement. Apoptosis in tissue sections was detected by TUNEL assay technique. Bleomycin administration induced fibrosis in skin and lung tissues. Severe apoptosis was seen in skin and lung tissues of the bleomycin-treated group (p&lt;0.001 in the skin and p&lt;0.05 in the lung). Progesterone injection either in the skin (p&gt;0.05) or in the lung (p&gt;0.05) did not alter apoptosis in bleomycin-treated animals. Our data confirm the role of apoptosis in the pathogenesis of fibrosis in this model; however, progesterone does not affect cellular apoptosis in skin and lung tissues of bleomycin-injured animals.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1857</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1857/1395</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>18</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Altered Expression of miR-326 in T Cell-derived Exosomes of Patients with Relapsing-remitting Multiple Sclerosis</title>
    <FirstPage>108</FirstPage>
    <LastPage>113</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Azimi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Immunology Research Center, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mojdeh</FirstName>
        <LastName>Ghabaee</LastName>
        <affiliation locale="en_US">Department of Neurology, Iranian Center of Neurological Research, Imam Khomeini Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abdolreza</FirstName>
        <LastName>Naser Moghadasi</LastName>
        <affiliation locale="en_US">Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Izad</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>03</Month>
        <Day>06</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
        <Month>06</Month>
        <Day>03</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Invasion of auto-reactive CD4+ T cells especially Th17 into central nervous system (CNS) is an underlying pathogenic mechanism in multiple sclerosis (MS). CD4+ T cells release exosomes which are enriched in microRNAs, reflective of cell&#x2019;s physiological or pathological condition. Thus exosomes could be potent agents to provide quantitative and qualitative information about involved cells in MS. We investigated the expression of pathogenic microRNAs in T cells-derived exosomes of MS patients or healthy controls. Conventional T cells (Tconv) derived from relapsing-remitting (RR) MS patients (n=10) and healthy controls (n=10) were purified and cultured for 3 days by soluble anti-CD3/CD28. Exosomes were purified from cultured-T cells supernatants. The expression levels of exosomal miR-146a, miR-29a, miR-155, and miR-326 were quantified by real-time PCR. A statistically significant increased expression of miR-326 in Tconv-derived exosomes was observed in RRMS patients as compared with controls (7.5&#xB1;1.88vs 2.51&#xB1;0.9 p=0.03), On the contrary, no differences were found in the expression levels of miR-155, miR-146a, and miR-29a, in Tconv-derived exosomes of &#xA0;patients as compared with controls (p&gt;0.05).&#xA0;Our results point to altered expression in exosome-derived microRNAs. MiR-326 was previously shown to play a role in the immunopathogenesis of MS by inducing TH17 differentiation and maturation. Therefore, miR-326 containing exosomes might also be a potential clinical target in course of MS. Moreover, the deregulation of this miRNA in exosomes may serve as a diagnostic and prognostic biomarker.&#xA0;</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/1891</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/1891/1399</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>18</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2019</Year>
        <Month>02</Month>
        <Day>24</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Immunomodulatory Effects of Human Adipose Tissue-derived Mesenchymal Stem Cells on T Cell Subsets in Patients with Rheumatoid Arthritis</title>
    <FirstPage>114</FirstPage>
    <LastPage>119</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Rasoul</FirstName>
        <LastName>Baharlou</LastName>
        <affiliation locale="en_US">Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran AND Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nesa</FirstName>
        <LastName>Rashidi</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abbas</FirstName>
        <LastName>Ahmadi-Vasmehjani</LastName>
        <affiliation locale="en_US">Department of Immunology and Microbiology, School of Medicine, Jahrom University of  Medical Sciences, Jahrom, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahshid</FirstName>
        <LastName>Khoubyari</LastName>
        <affiliation locale="en_US">Department of Student Research Committee, School of Medicine, Jahrom University  of Medical Sciences, Jahrom, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Sheikh</LastName>
        <affiliation locale="en_US">Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Saiedeh</FirstName>
        <LastName>Erfanian</LastName>
        <affiliation locale="en_US">Research Center for Non-Communicable Diseases, School of Medicine, Jahrom University of Medical Sciences, Jahrom, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2018</Year>
        <Month>06</Month>
        <Day>15</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2018</Year>
    