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Preserved MAIT cell numbers and function in idiopathic CD4 lymphocytopenia

  1. Author:
    Sortino,Ornella
    Dias, Joana
    Anderson, Megan
    Laidlaw, Elizabeth
    Leeansyah, Edwin
    Lisco, Andrea
    Sheikh, Virginia
    Sandberg, Johan K
    Sereti, Irini [ORCID]
  2. Author Address

    Clinical Research Directorate/Clinical Monitoring Leidos Research Program, Leidos Biomedical Research, Inc., National Cancer Institute Campus at Frederick, Frederick, Maryland, USA., National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA., Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden., Tsinghua-Berkeley Shenzhen Institute, Tsinghua University, Shenzhen, China.,
    1. Year: 2020
    2. Date: Dec 24
  1. Journal: The Journal of Infectious Diseases
    1. 224
    2. 4
    3. Pages: 715-725
  2. Type of Article: Article
  3. ISSN: 0022-1899
  1. Abstract:

    Mucosal-associated invariant T (MAIT) cells constitute a subset of unconventional, MR1-restricted T cells involved in antimicrobial responses as well as inflammatory, allergic, and autoimmune diseases. Chronic infection and inflammatory disorders as well as immunodeficiencies are often associated with decline and/or dysfunction of MAIT cells. We investigated the MAIT cells in patients with idiopathic CD4+ lymphocytopenia (ICL), a syndrome characterized by consistently low CD4 T-cell counts (< 300 cell/µL) in the absence of HIV infection or other known immunodeficiency, and by susceptibility to certain opportunistic infections. The numbers, phenotype, and function of MAIT cells in peripheral blood were preserved in ICL patients compared to healthy controls. Administration of interleukin-7 (IL-7) to ICL patients expanded the CD8+ MAIT-cell subset, with maintained responsiveness and effector functions after IL-7 treatment. ICL patients maintain normal levels and function of MAIT cells, preserving some antibacterial responses despite the deficiency in CD4+ T cells. NCT00867269. Published by Oxford University Press for the Infectious Diseases Society of America 2020.

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External Sources

  1. DOI: 10.1093/infdis/jiaa782
  2. PMID: 33367864
  3. WOS: 000703928000019
  4. PII : 6047591

Library Notes

  1. Fiscal Year: FY2020-2021
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