<?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>8</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2009</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Coxsackievirus B3 Infection Induced Viral Myocarditis by Regulating the Expression Pattern of Chemokines in Cardiac Myocytes</title>
    <FirstPage>1</FirstPage>
    <LastPage>9</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Shen</FirstName>
        <LastName>Yan</LastName>
        <affiliation locale="en_US">The First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, People&#x2019;s Republic of China</affiliation>
      </Author>
      <Author>
        <FirstName>Cheng Kan</FirstName>
        <LastName>Quan</LastName>
        <affiliation locale="en_US">The First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, People&#x2019;s Republic of China</affiliation>
      </Author>
      <Author>
        <FirstName>Wei Chu</FirstName>
        <LastName>Yi</LastName>
        <affiliation locale="en_US">Department of Immunology, Shanghai Medical College of Fudan University, Shanghai 200032,</affiliation>
      </Author>
      <Author>
        <FirstName>Dong Xiong</FirstName>
        <LastName>Si</LastName>
        <affiliation locale="en_US">Department of Immunology, Shanghai Medical College of Fudan University, Shanghai 200032,</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Viral myocarditis is a common cardiovascular disease, which has greatly threatened human health. However, up to now, the pathogenesis of viral myocarditis has been unclear, which leads to the lack of its effective treatments. 
To investigate the role of chemokines in pathogenesis of viral myocarditis, mRNA expression for a panel of 19 chemokines detected by RT-PCR in myocardial tissue of BALB/c mice that were inoculated intraperitoneally with coxsackievirus B3. Moreover primary cultured cardiac myocytes were infected with coxsackievirus B3 following extraction of RNA, from myocytes the expression of 19 chemokines was detected by by RT-PCR. 
Our results showed that there was much difference in the expression pattern of chemokines in myocardial tissue between infected mice with viral myocarditis and uninfected control mice. The expression of chemokines was varied significantly in clusters in myocardium post coxsackievirus B3 infection. There were also complexity and imbalance in the change of the expression of chemokines. In the meantime, Coxsackievirus B3 infection also influenced the expression pattern of chemokines in cardiac myocytes in vitro. However the expression of monocyte chemoattractant protein-1 alone was upregulated in cardiac myocytes post coxsackievirus B3 infection in the 19 detected chemokines. 
The chemokine expression pattern changed in complexity and imbalance manner both in myocardium and in primary cultured cardiac myocytes after coxsackievirus B3 infection. Coxsackievirus B3 infection may start viral myocarditis by regulating the expression pattern of chemokines in cardiac myocytes. MCP-1 may be one of key chemokines in the initial stage of viral myocarditis.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/227</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/227/227</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>8</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2009</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Effect of Nicotinamide on Experimental Induced Diabetes</title>
    <FirstPage>11</FirstPage>
    <LastPage>18</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Q. Alenzi</FirstName>
        <LastName>Faris</LastName>
        <affiliation locale="en_US">Department of Clinical Laboratory Sciences, College of Applied Medical Sciences,</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Insulin dependent diabetes mellitus (IDDM) results from irreversible loss of beta cells (&#x3B2;-cells) of the pancreas. A Streptozotocin (STZ)-induced diabetes in animal model mimics, in some aspects, recent onset IDDM. This study was conducted to investigate the effect of nicotinamide on experimentally-induced IDDM. 
Thirty Spraque Dawley rats were divided into 3 groups; a control group, a diabetic group which received an intraperitoneal (i.p.) injection of 55 mg/kg STZ and a nicotinamide group (1g/kg/day) which were dosed orally for 3 days followed by (i.p.) STZ (55 mg/kg) with the nicotinamide treatment continuing for an additional 14 days. 
Rats receiving STZ became diabetic after 2 weeks. This diabetic group showed hyperglycemia, and a very low level of C-peptide. Furthermore, pancreatic islets exhibited increased nitric oxide (NO) production together with an increased apoptotic index (as detected by TUNEL and electron microscopy). Nicotinamide treatment prevented STZ-induced diabetes, it also antagonized an increase in NO, and inhibited &#x3B2;-cell apoptosis. Fasting blood glucose, serum insulin and serum C-peptide were all within the normal range in the nicotinamide group. 
The nicotinamide protection of &#x3B2;-cells may be facilitated via inhibition of apoptosis and nitric oxide generation. It is suggested that nicotinamide might be considered an effective agent for the prevention and treatment of IDDM in prediabetic, and early stages, of IDDM.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/228</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/228/228</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>8</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2009</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Substance P Potentiates TGF-&#xF062;1 Production in Lung Epithelial Cell Lines</title>
    <FirstPage>19</FirstPage>
    <LastPage>24</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Yaraee</FirstName>
        <LastName>Roya</LastName>
        <affiliation locale="en_US">Department of Immunology, Immunoregulation Research Group, Medical Research Center, Medical School,</affiliation>
      </Author>
      <Author>
        <FirstName>Ghazanfari</FirstName>
        <LastName>Tooba</LastName>
        <affiliation locale="en_US">Department of Immunology, Immunoregulation Research Group, Medical Research Center, Medical School,</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Transforming growth factor-beta (TGF-&#x3B2;) is one of the most important cytokines implicated in growth, differentiation, repair and also the pathogenesis of the lung fibrosis by its stimulatory effect on extracellular matrix deposition. Pulmonary epithelial cells are considered as a source of TGF-&#x3B2; in lung. Substance P (SP), as a neuroimmunomodulator has elevated levels in inflamed airways and although it has significant role in the pathogenesis of the lung fibrosis, but its effect on transforming growth factor -beta (TGF-&#x3B2;) production of the lung epithelial cells (and so its regulatory potential) remains unclear. 
In this study TGF-&#xF062;1 levels in supernatants of the normal (BEAS-2B) and cancerous (A549) lung epithelial cell line cultures at the presence of various concentrations of SP were examined and MTT assay was performed to evaluate cells viability. 
We have observed that SP (without any other stimulator) significantly augments TGF-&#x3B2; production of both BEAS and A54 cells and this effect is inhibited by NK1-receptor antagonist (CP-96345). We have also observed that the viability of cells did not significantly affect at the presence of SP. 
It can be concluded that SP can directly modulate the release of TGF-&#x3B2; from human bronchial epithelial cell line and thereby participates in various lung functions or pathologic conditions.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/229</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/229/229</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>8</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2009</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Generation of Immune Inhibitory Dendritic Cells and</title>
    <FirstPage>25</FirstPage>
    <LastPage>30</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Abediankenari</FirstName>
        <LastName>Saeid</LastName>
        <affiliation locale="en_US">Department of Microbiology and Immunology, School of Medicine,</affiliation>
      </Author>
      <Author>
        <FirstName>Ghasemi</FirstName>
        <LastName>Maryam</LastName>
        <affiliation locale="en_US">2 Department of Pathology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Variety of positive as well as negative regulatory signals are provided by antigen presenting cell in particular by dendritic cells. In this research, we studied the capacity of dendritic cells to expand antigen-specific T regulatory cells.We also investigated the role of TGF-beta in induction inhibitory functions of dendritic cells in mixed leukocyte reactions.
Dendritic cells were generated from blood CD14+ monocytes with granulocyte-Monocyte colony stimulating factor and interleukin-4 with or without TGF-beta (TGF-&#x3B2;-GM-DC or GM-DC). CD4+ T cell were isolated to assess lymphocyte proliferation by lymphocyte transformation test assay and the ratio of CD4+FOXp3+ CD25+ T cells were determined by fluorescene-activated cell sorter. 
T cell proliferation responses in GM-DC showed a significance antigen-specific proliferative response comparing with TGF&#x3B2;-GM -DC. T Cell proliferation was inhibited in co-culture system containing DC-treated TGF-&#x3B2;. 
It can be suggested that the expsansion of T regulatory by TGF-&#x3B2;-GM-DC provides a means for antigen specific control of unwanted immune reactions.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/230</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/230/230</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>8</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2009</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Association of Cytokine Gene Polymorphisms with Chronic Obstructive</title>
    <FirstPage>31</FirstPage>
    <LastPage>42</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Trajkov</FirstName>
        <LastName>Dejan</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Stojkovikj</FirstName>
        <LastName>Jagoda Mirkovska</LastName>
        <affiliation locale="en_US">Clinic for Pulmoallergology, University School of Medicine "Ss. Kiril and Metodij", Skopje, Republic</affiliation>
      </Author>
      <Author>
        <FirstName>Petlichkovski</FirstName>
        <LastName>Aleksandar</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Strezova</FirstName>
        <LastName>Ana</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Mladenovska</FirstName>
        <LastName>Olivija Efinska</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Sandevska</FirstName>
        <LastName>Emilija</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Sibinovska</FirstName>
        <LastName>Olgica</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Hristomanova</FirstName>
        <LastName>Slavica</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Djulejic</FirstName>
        <LastName>Eli</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Petrov</FirstName>
        <LastName>Jordan</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
      <Author>
        <FirstName>Gogusev</FirstName>
        <LastName>Jean</LastName>
        <affiliation locale="en_US">INSERM U507, H&#xF4;pital Necker-Enfants Malades, Paris, France</affiliation>
      </Author>
      <Author>
        <FirstName>Spiroski</FirstName>
        <LastName>Mirko</LastName>
        <affiliation locale="en_US">Institute of Immunobiology and Human Genetics, University School of Medicine "Ss. Kiril and Metodij"</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">The aim of this study was to examine the association of 22 cytokine gene polymorphism in Macedonians with chronic obstructive pulmonary disease (COPD). 
The sample of the population comprised of 301 normal respondents and 62 patients with COPD. Cytokine genotyping was performed by polymerase chain reaction with sequence-specific priming (PCR-SSP). 
Positive (susceptible) association was found between patient with COPD and IL-1&#x3B1; -889/C allele; where as negative (protective) association among was found for the following alleles IL-1&#x3B2; +3962/C; IL-12B -1188/A; IFN&#x3B3; +874/T; IL-2 -330/G; IL-4 -1098/G and IL-4-33/C. We found positive (susceptible) association between patients with COPD and following genotypes: IL4 -33/T:T; IFN&#x3B3; +874/A:A; IL-4 -1098/T:T ; IL-1&#x3B1; -889/C:C; IL-1&#x3B2; +3962/C:T; IL-12B -1188/C:C; IL-4R&#x3B1; +1902/G:G; IL-10 -1082/G:G; IL-2 -330/T:T; IL-4 -590/C:C; and IL-1&#x3B1; -889/C:T. Negative (protective) association between patients with COPD and following genotypes was found: IFN&#x3B3; +874/A:T; IL-4 -33/C:T; IL-4 -1098/G:T; IL-2 -330/G:T; IL-1&#x3B2; +3962/C:T; IL-4 -590/C:T; IL-10 -1082/A:G; and IL-4 -33/C:C. Positive (susceptible) association between patients with COPD and following haplotypes was found: IL-4/TCT; IL-10/ATC; and IL-2/TG, and negative (protective) association was found between the patients with COPD and haplotypes for: IL-4/TTC; and IL-4/GCC. 
It could be concluded that several cytokine polymorphisms are positively (susceptible), or negatively (protective) associated with COPD in Macedonians.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/231</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/231/231</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>8</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2009</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Neutropenia Associated with X-Linked Agammaglobulinemia</title>
    <FirstPage>43</FirstPage>
    <LastPage>47</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Aghamohammadi</FirstName>
        <LastName>Asghar</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Children's Medical Center, Tehran University of Medical Sciences, Tehran,</affiliation>
      </Author>
      <Author>
        <FirstName>Cheraghi</FirstName>
        <LastName>Taher</LastName>
        <affiliation locale="en_US">Growth and Development Research Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Rezaei</FirstName>
        <LastName>Nima</LastName>
        <affiliation locale="en_US">Immunology, Asthma and Allergy Research Institute, Tehran University of Medical Sciences, Tehran, I</affiliation>
      </Author>
      <Author>
        <FirstName>Kanegane</FirstName>
        <LastName>Hirokazu</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Graduate School of Medicine, University of Toyama, Toyama, Japan</affiliation>
      </Author>
      <Author>
        <FirstName>Abdollahzede</FirstName>
        <LastName>Sina</LastName>
        <affiliation locale="en_US">Growth and Development Research Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Talaei-Khoei</FirstName>
        <LastName>Mojtaba</LastName>
        <affiliation locale="en_US">Growth and Development Research Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Heidari</FirstName>
        <LastName>Golnaz</LastName>
        <affiliation locale="en_US">Growth and Development Research Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zandieh</FirstName>
        <LastName>Fariborz</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Children's Medical Center, Tehran University of Medical Sciences, Tehran,</affiliation>
      </Author>
      <Author>
        <FirstName>Moin</FirstName>
        <LastName>Mostafa</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Children's Medical Center, Tehran University of Medical Sciences, Tehran,</affiliation>
      </Author>
      <Author>
        <FirstName>Miyawaki</FirstName>
        <LastName>Toshio</LastName>
        <affiliation locale="en_US">Department of Pediatrics, Graduate School of Medicine, University of Toyama, Toyama, Japan</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">X-linked Agammaglobulinemia (XLA) is a hereditary immunodeficiency, characterized by an early onset of recurrent bacterial infections, hypogammaglobulinemia and markedly reduced B lymphocytes number. 
In order to determine the association of neutropenia among Iranian patients with XLA, hospital records of 30 patients with confirmed XLA in Children Medical Center Hospital, were reviewed. 
Eight out of 30 XLA patients (26.7%) developed neutropenia during the course of the disease. In two patients, episodes of neutropenia were identified before or at the time of diagnosis of XLA. Other six patients whom were not visited regularly and did not receive periodical immunoglobulin replacement therapy experienced neutropenia after diagnosis of XLA. 
Neutropenia in XLA is mainly associated with infection and is resolved with intravenous immunoglobulin replacement and antibiotics therapy.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/232</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/232/232</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>8</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2009</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Antinuclear Antibodies in Asthma Patients- A Special Asthma Phenotype?</title>
    <FirstPage>49</FirstPage>
    <LastPage>52</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Agache</FirstName>
        <LastName>Ioana</LastName>
        <affiliation locale="en_US">Transylvania University, Faculty of Medicine, Department of Allergy and Clinical Immunology, Romania</affiliation>
      </Author>
      <Author>
        <FirstName>Duca</FirstName>
        <LastName>Liliana</LastName>
        <affiliation locale="en_US">Transylvania University, Faculty of Medicine, Department of Allergy and Clinical Immunology, Romania</affiliation>
      </Author>
      <Author>
        <FirstName>Anghel</FirstName>
        <LastName>Mariana</LastName>
        <affiliation locale="en_US">Brasov County Hospital, Immunology Laboratory, Romania</affiliation>
      </Author>
      <Author>
        <FirstName>Pamfil</FirstName>
        <LastName>Gheorghe</LastName>
        <affiliation locale="en_US">Transylvania University, Faculty of Medicine, Department of Biostatistics, Romania</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Several studies reported the appearance of asthma and autoimmune conditions in the same patient, but the clinical significance of this association was not yet assessed. 
One hundred asthmatic patients were observed for one year evolution with death, severe exacerbations, intake of &gt; 1000 micrograms of beclometasone or equivalent (high ICS) and FEV1 decline &gt;100 ml, in relation with ANA (ELISA), sputum and blood eosinophilia (EO), NSAID intolerance, BMI &gt;25, chronic rhinosinusitis, smoking status and FEV1 100 ml/year). Multiple regression analysis pointed out several different independent risk factors for severe asthma evolution: for death presence of ANA (P=0.037), NSAID intolerance (P25 (P=0.046) and NSAID intolerance (P=0.017)
The presence of ANA is an independent risk factbody against A subunit could be a useful tool for immunological diagnosis of STEC induced infection.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/291</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/291/291</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>10</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2011</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Health-Related Quality of Life in Primary Antibody Deficiency</title>
    <FirstPage>47</FirstPage>
    <LastPage>51</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Asghar</FirstName>
        <LastName>Aghamohammadi</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ali</FirstName>
        <LastName>Montazeri</LastName>
        <affiliation locale="en_US">Iranian Institute for Health Sciences Research, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hassan</FirstName>
        <LastName>Abolhassani</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sepideh</FirstName>
        <LastName>Saroukhani</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sarvenaz</FirstName>
        <LastName>Pourjabbar</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mahmoud</FirstName>
        <LastName>Tavassoli</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Behzad</FirstName>
        <LastName>Darabi</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Amir</FirstName>
        <LastName>Imanzadeh</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nima</FirstName>
        <LastName>Parvaneh</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nima</FirstName>
        <LastName>Rezaei</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiency, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran AND</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Patients&#xA0; with&#xA0; primary&#xA0; antibody&#xA0; deficiencies&#xA0; (PAD)&#xA0; are&#xA0; susceptible&#xA0; to&#xA0; recurrent&#xA0; and chronic infections and a variety of complications. This study was performed to assess quality of life (QoL) of PAD patients who were under long term treatment and regular follow-up.Thirty six adults with proved diagnosis of PAD, who had received regular intravenous immunoglobulin replacement therapy, were enrolled in this study. The QoL of selected PAD patients was measured by Medical Outcomes Study 36-item Short-Form (SF-36) Health Survey questionnaire.
The patients with PAD showed significantly reduced scores in physical component in comparison&#xA0; with&#xA0; healthy&#xA0; age-sex&#xA0; matched&#xA0; control&#xA0; subjects&#xA0; (60.2&#xB1;20.1&#xA0; vs.&#xA0; 85.5&#xB1;4.7, P&lt;0.001). Mental component score was also significantly decreased in the patient's group (59.8&#xB1;19.5 vs. 72.3&#xB1;3.4, P=0.002). There was a reverse association between SF-36 scores and number of infections episodes (r=-0.73 P=0.003). The patients with long delay diagnosis showed significantly lower SF-36 scores (r=-0.62, P=0.003).
The patients with PAD who were diagnosed timely and managed appropriately seem to have lower complications and better QoL. However, the patients with severe phenotypes and long delay in diagnosis showed lower QoL, even in medical management.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/292</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/292/292</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>10</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2011</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Schwann Cell Apoptosis and p75NTR siRNA</title>
    <FirstPage>53</FirstPage>
    <LastPage>59</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Masoumeh</FirstName>
        <LastName>Firouzi</LastName>
        <affiliation locale="en_US">Department of Biochemistry, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran AND Tissue Repair Lab, Institute of Biochemistry and Biophysics, University of Tehran AND Research Centre for Neural Repair, University of Tehran</affiliation>
      </Author>
      <Author>
        <FirstName>Farzaneh</FirstName>
        <LastName>Sabouni</LastName>
        <affiliation locale="en_US">Department of Biochemistry, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Abdolkhaleg</FirstName>
        <LastName>Deezagi</LastName>
        <affiliation locale="en_US">Department of Biochemistry, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Zahra</FirstName>
        <LastName>Hassannejad Pirbasti</LastName>
        <affiliation locale="en_US">Tissue Repair Lab, Institute of Biochemistry and Biophysics, University of Tehran AND Research Centre for Neural Repair, University of Tehran</affiliation>
      </Author>
      <Author>
        <FirstName>Fatemeh</FirstName>
        <LastName>Poorrajab</LastName>
        <affiliation locale="en_US">Tissue Repair Lab, Institute of Biochemistry and Biophysics, University of Tehran</affiliation>
      </Author>
      <Author>
        <FirstName>Vafa</FirstName>
        <LastName>Rahimi-Movaghar</LastName>
        <affiliation locale="en_US">Sina Trauma and Surgery Research Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">The p75 pan-neurotrophin receptor (p75NTR) plays a pivotal role in linking the immune system with the nervous system. p75NTR is required for the development of several characteristic features of allergic asthma. Also p75NTR upregulated by reactive Schwann cells after peripheral nerve injury. 
Moreover p75NTR and RhoA play a critical role in the regulation of apoptosis. To determine whether the designed siRNA for p75NTR can downregulates both p75NTR and Rho-A at RNA level in rats and, if so, at what magnitude, Schwann cell apoptosis occurs. Isolation and purification of neonate Schwann cells were prepared from rat sciatic nerve. Specific siRNA duplex was designed for p75NTR.
To investigate the role of siRNA-mediated knockdown of p75NTR, the gene expression in p75NTR was examined with reverse transcription-polymerase chain reaction (RT-PCR) and Real-Time RT-PCR. Schwann cell apoptosis was performed by Annexin and TUNEL assays after 24 hours. Following p75NTR Transfection siRNA, p75NTR gene, compared with control, was downregulated by 73%. Without using siRNA for Rho-A, Rho-A gene was downregulated by 89% at the same time. Based on Annexin assay, apoptosis of Schwann cells occurred in siRNA+NGF and control+NGF by 16.76%&#xB1;2.27 and 92.39%&#xB1;1.82, respectively. 
TUNEL data showed that apoptosis of Schwann cells occurred in siRNA and control by 12.91%&#xB1;6.39 and 78.55%&#xB1;11.85, respectively. Thus, p75-siRNA downregulated both p75NTR and Rho-A at RNA level in rats and showed a role on decreased cell apoptosis compared to the controls.</abstract>
    <web_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/view/293</web_url>
    <pdf_url>https://ijaai.tums.ac.ir/index.php/ijaai/article/download/293/293</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>10</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="epublish">
        <Year>2011</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Family Functioning and Illness Perception of Parents of Children with Atopic Dermatitis, Living without Skin Symptoms, but with Psychosomatic Symptoms</title>
    <FirstPage>61</FirstPage>
    <LastPage>65</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Alain. R</FirstName>
        <LastName>Rodr&#xED;guez-Orozco</LastName>
        <affiliation locale="en_US">Divisi&#xF3;n de Posgrado, Facultad de Medicina &#x201C;Dr Ignacio Ch&#xE1;vez&#x201D;, Universidad Michoacana de San Nicol&#xE1;s De Hidalgo, Morelia, Michoac&#xE1;n, M&#xE9;xico AND Instituto de Investigaci&#xF3;n Cient&#xED;fica en Temas de Familia, Alergia e Inmunolog&#xED;a, Morelia, Michoac&#xE1;n, M&#xE9;xico</affiliation>
      </Author>
      <Author>
        <FirstName>E. G.</FirstName>
        <LastName>Kan&#xE1;n-Cede&#xF1;o</LastName>
        <affiliation locale="en_US">Instituto de Investigaci&#xF3;n Cient&#xED;fica en Temas de Familia, Alergia e Inmunolog&#xED;a, Morelia, Michoac&#xE1;n, M&#xE9;xico AND Facultad de Psicolog&#xED;a, Universidad Michoacana de San Nicol&#xE1;s De Hidalgo, Morelia, Michoac&#xE1;n, M&#xE9;xico, Instituto de Investigaci&#xF3;n Cient&#xED;fica en Temas de Familia, Alergia e Inmunolog&#xED;a. Morelia, Michoac&#xE1;n, M&#xE9;xico</affiliation>
      </Author>
      <Author>
        <FirstName>E. Guill&#xE9;n</FirstName>
        <LastName>Mart&#xED;nez</LastName>
        <affiliation locale="en_US">Facultad de Psicolog&#xED;a, Universidad Michoacana de San Nicol&#xE1;s De Hidalgo, Morelia, Michoac&#xE1;n, M&#xE9;xico</affiliation>
      </Author>
      <Author>
        <FirstName>M. J</FirstName>
        <LastName>Campos Garibay</LastName>
        <affiliation locale="en_US">Facultad de Psicolog&#xED;a, Universidad Michoacana de San Nicol&#xE1;s De Hidalgo, Morelia, Michoac&#xE1;n, M&#xE9;xico</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Emotional factors and a recurrent psychosomatic env