<?xml version="1.0"?>
<Articles JournalTitle="Immunology and Genetics Journal">
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Immunology and Genetics Journal</JournalTitle>
      <Issn>2645-4831</Issn>
      <Volume>4</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="epublish">
        <Year>2021</Year>
        <Month>09</Month>
        <Day>22</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">DNA Methylation of JAK2 Gene in Intestinal Biopsy and Peripheral Blood Samples of Patients with Ulcerative Colitis</title>
    <FirstPage>155</FirstPage>
    <LastPage>160</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Sara</FirstName>
        <LastName>Hanaei</LastName>
        <affiliation locale="en_US">Department of Neurosurgery, Imam Khomeini Hospital Complex (IKHC), Tehran University of Medical Sciences (TUMS), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Golshid</FirstName>
        <LastName>Sanati</LastName>
        <affiliation locale="en_US">Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>Sadr</LastName>
        <affiliation locale="en_US">Molecular Immunology Research Center, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Safoora</FirstName>
        <LastName>Gharibzadeh</LastName>
        <affiliation locale="en_US">Department of Epidemiology and Biostatistics, Research Centre for Emerging and Reemerging Infectious Diseases, Pasteur Institute of Iran, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Roham</FirstName>
        <LastName>Salmanroghani</LastName>
        <affiliation locale="en_US">School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Hassan</FirstName>
        <LastName>Salmanroghani</LastName>
        <affiliation locale="en_US">Department of Gastrointestinal Diseases, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nima</FirstName>
        <LastName>Rezaei</LastName>
        <affiliation locale="en_US">Tehran University of Medical Sciences</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>12</Month>
        <Day>29</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2023</Year>
        <Month>02</Month>
        <Day>27</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Background and Aims: Comprised of two main subtypes (Ulcerative Colitis (UC) and Crohn), inflammatory bowel disease is caused by an interaction between genetic and environmental factors. As of the important role of innate immunity and JAK/STAT signaling pathway, the current study was designed to investigate the methylation status JAK2 gene in blood and tissue samples of patients with UC.
&#xD;

Methods: Genomic DNA was extracted from blood and intestinal biopsy samples of 28 UC patients and 28 controls. After bisulfite DNA conversion, real-time quantitative multiplex methylation specific PCR (QM-MSP) method was applied in order to assess JAK2 promotor methylation status.
&#xD;

Results: The JAK2 promotor in the intestinal biopsy samples was significantly hypermethylated in UC as the mean of unmethylated DNA was 1.255&#xB1;1.865 in the patients group, while it was 1.292&#xB1;4.726 in control group (P=0.002).
&#xD;

Conclusions: Hypermathylation of JAK2 gene may play a part in pathophysiology of UC which could result in gene silencing.</abstract>
    <web_url>https://igj.tums.ac.ir/index.php/igj/article/view/112</web_url>
    <pdf_url>https://igj.tums.ac.ir/index.php/igj/article/download/112/79</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Immunology and Genetics Journal</JournalTitle>
      <Issn>2645-4831</Issn>
      <Volume>4</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="epublish">
        <Year>2021</Year>
        <Month>09</Month>
        <Day>22</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Omenn Syndrome Caused by A Novel Mutation of the DCLRE1C Gene: Case Report and Review of Literature</title>
    <FirstPage>132</FirstPage>
    <LastPage>137</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Taher</FirstName>
        <LastName>Cheraghi</LastName>
        <affiliation locale="en_US">17th Shahrivar Children&#x2019;s Hospital, Department of Pediatrics, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Afshin</FirstName>
        <LastName>Safaee</LastName>
        <affiliation locale="en_US">17th Shahrivar Children&#x2019;s Hospital, Department of Pediatrics, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Ebrahim</FirstName>
        <LastName>Esmaili</LastName>
        <affiliation locale="en_US">17th Shahrivar Children&#x2019;s Hospital, Department of Pediatrics, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>kiomars</FirstName>
        <LastName>Golshekan</LastName>
        <affiliation locale="en_US">17th Shahrivar Children&#x2019;s Hospital, Department of Pediatrics, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Maryam</FirstName>
        <LastName>ghavideldarestani</LastName>
        <affiliation locale="en_US">Hull York Medical School, Cottingham Road, Hull, HU67RX, UK</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>03</Month>
        <Day>02</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>08</Month>
        <Day>24</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">We report a case of Omenn syndrome due to a novel mutation of the gene DCLRE1C(Artemis). He was referred to our hospital with a complaint of protracted diarrhea, erythematoexfoliative rash, urinary tract infection, pneumonia, and failure to thrive. He was 2 months old. At the first sight, the diagnoses of Omenn syndrome, graft versus host disease (GVHD), Netherton syndrome, and Atopic dermatitis came to mind. Laboratory evaluation showed lymphopenia, eosinophilia, high IgE, and whole-exome sequencing revealed a mutation of the DCLRE1C gene. After obtaining blood samples, he received broad-spectrum antibiotics, antifungals, antiviral, prophylaxis for pneumocystis Jirovecii pneumonia, and Intravenous immunoglobulin. He expired owing to delayed referral and overwhelming sepsis before receiving bone marrow transplantation. In every neonate infant presenting with erythematoexfoliative skin rash, refractory infection, and lymphopenia, Omenn syndrome should be considered.</abstract>
    <web_url>https://igj.tums.ac.ir/index.php/igj/article/view/96</web_url>
    <pdf_url>https://igj.tums.ac.ir/index.php/igj/article/download/96/77</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Immunology and Genetics Journal</JournalTitle>
      <Issn>2645-4831</Issn>
      <Volume>4</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="epublish">
        <Year>2021</Year>
        <Month>09</Month>
        <Day>22</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The novel ZBTB24 mutation identified in an Iranian patient with type 2 ICF syndrome</title>
    <FirstPage>166</FirstPage>
    <LastPage>170</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Saba</FirstName>
        <LastName>Arshi</LastName>
        <affiliation locale="en_US">1.	Department of Allergy and Clinical Immunology, Rasool e Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad</FirstName>
        <LastName>Nabavi</LastName>
        <affiliation locale="en_US">1.	Department of Allergy and Clinical Immunology, Rasool e Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Mohammad Hasan</FirstName>
        <LastName>Bemanian</LastName>
        <affiliation locale="en_US">1.	Department of Allergy and Clinical Immunology, Rasool e Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Morteza</FirstName>
        <LastName>Fallahpour</LastName>
        <affiliation locale="en_US">1.	Department of Allergy and Clinical Immunology, Rasool e Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Samaneh</FirstName>
        <LastName>Delavari</LastName>
        <affiliation locale="en_US">Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Science, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nima</FirstName>
        <LastName>Rezaei</LastName>
        <affiliation locale="en_US">2.	Research Center for Primary Immunodeficiencies, Pediatrics Center of Excellence, Children&#x2019;s Medical Center, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Sima</FirstName>
        <LastName>Shokri</LastName>
        <affiliation locale="en_US">1.	Department of Allergy and Clinical Immunology, Rasool e Akram Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2023</Year>
        <Month>01</Month>
        <Day>02</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2023</Year>
        <Month>02</Month>
        <Day>27</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Autosomal-recessive immunodeficiency, centromeric instability, and facial anomalies (ICF) syndrome is mainly determined by recurrent tract respiratory and gastrointestinal infections in early childhood due to agammaglobulinemia. Most patients with ICF syndrome die of infection at a young age, usually in the first or second decade of life. The leading cause of ICF disorders is mutations in genes whose products play a role in DNA methylation. ICF syndrome is classified into two groups: type 1 (ICF1) patients have mutations in the DNMT3B gene, and about half of type 2 (ICF2) patients have mutations in the ZBTB24 gene. In this study, we report the case of a 34-year-old female of Iranian consanguineous parents, who was diagnosed at one year of age with ICF-2 syndrome with recurrent infections, mental retardation, and a homozygous novel mutation in the ZBTB24 gene.</abstract>
    <web_url>https://igj.tums.ac.ir/index.php/igj/article/view/116</web_url>
    <pdf_url>https://igj.tums.ac.ir/index.php/igj/article/download/116/81</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Immunology and Genetics Journal</JournalTitle>
      <Issn>2645-4831</Issn>
      <Volume>4</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="epublish">
        <Year>2021</Year>
        <Month>09</Month>
        <Day>22</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">The Role of Intranasal Corticosteroid Therapy on Pediatric Adenoidal Hypertrophy: A Randomized Clinical Trial Study</title>
    <FirstPage>161</FirstPage>
    <LastPage>165</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Mahnaz</FirstName>
        <LastName>Sadeghi-Shabestari</LastName>
        <affiliation locale="en_US">Tuberculosis and lung disease research center, immunology research center of Tabriz ,children hospital ,Tabriz university of medical science , Tabriz, Iran.</affiliation>
      </Author>
      <Author>
        <FirstName>Masoud</FirstName>
        <LastName>Naderpoor</LastName>
        <affiliation locale="en_US">Specialist in Otolaryngology ,  Tabriz university of medical science ,  Tabriz, Iran.</affiliation>
      </Author>
      <Author>
        <FirstName>Samira</FirstName>
        <LastName>Farzipour</LastName>
        <affiliation locale="en_US">Cardiologist, Tabriz university of medical science ,  Tabriz, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Azar</FirstName>
        <LastName>Dastranji</LastName>
        <affiliation locale="en_US">Pediatric pulmonology ,Tabriz university of medical science , Tabriz, Iran.</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>03</Month>
        <Day>02</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>06</Month>
        <Day>12</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">&#xA0;Background:Adenoidal hypertrophy (AH) is a common disorder in pediatric population with severe complications due to nasal air way obstruction. Adenoidectomy is a choice treatment for children with severe symptoms due to AH, however; it is accompanied with several side effects such as complication of surgery and emotional distress. We evaluated the efficacy of intranasal corticosteroid (Fluticasone) therapy on size and symptoms of Adenoid Hypertrophy.
&#xD;

Methods: In this clinical trial 45children with AH (2-14 years old) were enrolled. All of them underwent 8 weeks course of intranasal Fluticasone therapy and their symptoms before and after treatment were scored and also compared by questionnaires. They were divided into Atopic and non- Atopic groups and these two groups were compared with each other after treatment according to their response to therapy.
&#xD;

Results: After 8 weeks treatment with intra nasal fluticasone, improvement in all symptoms score of AH including (Snoring , Sleep Apnea ,Mouth breathing and Nasal congestion) &#xA0;was statistically significant(p=0.000). Significant improvement after treatment was observed in atopic patients and 92% of them (36 of 39) showed decrease clinical symptom of AH however this number in non-atopic patients was 50% (p value =0.024).
&#xD;

&#xA0;Conclusion: Our study demonstrates that an 8 weeks treatment with intranasal corticosteroid (Fluticasone) is associated with decrease in size of AH and all symptoms of obstruction. So intranasal corticosteroid therapy can prevent of adenoidectomy especially in atopic patients.</abstract>
    <web_url>https://igj.tums.ac.ir/index.php/igj/article/view/94</web_url>
    <pdf_url>https://igj.tums.ac.ir/index.php/igj/article/download/94/80</pdf_url>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Immunology and Genetics Journal</JournalTitle>
      <Issn>2645-4831</Issn>
      <Volume>4</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="epublish">
        <Year>2021</Year>
        <Month>09</Month>
        <Day>22</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Bacteriophage Therapy as An Alternative to Antibiotics: A Dead End or A Solution?</title>
    <FirstPage>138</FirstPage>
    <LastPage>154</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Amirhossein</FirstName>
        <LastName>Rismanbaf</LastName>
        <affiliation locale="en_US">Cellular and molecular undergraduate student, Faculty of Modern Sciences, Islamic Azad University of Medical Sciences, Tehran, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>07</Month>
        <Day>18</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>11</Month>
        <Day>01</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Antibiotic resistance has been around for years and could lead to a serious crisis in the near future. If the problem of antibiotic resistance is not solved, it is estimated that the increase in antimicrobial resistance would kill 10 million people a year by 2050 (more than the number of cancer deaths) and cost the world economy about 100 trillion USD, which will require immediate development of alternative treatments (1) (2). This problem prompted scientists to find a solution; one of these strategies is the use of bacteriophages as an alternative to antibiotics. In this review article, I will first focus on bacteriophages from various aspects and then, by analyzing the available information, I will try to answer the following questions:
&#xD;
&#xD;
&#x2022; Given the meager standard clinical data and characteristics of bacteriophages, is bacteriophage therapy a safe and reliable method?
&#xD;
&#x2022; Given the short time left before the antibiotic resistance crisis, is it cost-effective to invest in bacteriophage?
&#xD;
&#x2022; Are bacteriophages a double-edged sword? (Besides being used to treat bacterial diseases in the future, do bacteriophages have the potential to become a human virus in the future?)</abstract>
    <web_url>https://igj.tums.ac.ir/index.php/igj/article/view/100</web_url>
    <pdf_url>https://igj.tums.ac.ir/index.php/igj/article/download/100/78</pdf_url>
  </Article>
</Articles>
