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Th1 Differentiation Drives the Accumulation of Intravascular, Non-protective CD4 T Cells during Tuberculosis.

  1. Author:
    Sallin, Michelle A
    Sakai, Shunsuke
    Kauffman, Keith D
    Young, Howard
    Zhu, Jinfang
    Barber, Daniel L

  2. Author Address

    T-Lymphocyte Biology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA., Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA., Molecular and Cellular Immunoregulation Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA., T-Lymphocyte Biology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: barberd@niaid.nih.gov.,
    1. Year: 2017
    2. Date: Mar 28
  2. Journal: Cell reports
    1. 18
    2. 13
    3. Pages: 3091-3104
  4. Type of Article: Article
  5. Article Number: 3091-3104
  1. Abstract:

    Recent data indicate that the differentiation state of Th1 cells determines their protective capacity against tuberculosis. Therefore, we examined the role of Th1-polarizing factors in the generation of protective and non-protective subsets of Mtb-specific Th1 cells. We find that IL-12/23p40 promotes Th1 cell expansion and maturation beyond the CD73(+)CXCR3(+)T-bet(dim) stage, and T-bet prevents deviation of Th1 cells into Th17 cells. Nevertheless, IL- 12/23p40 and T-bet are also essential for the production of a prominent subset of intravascular CX3CR1(+)KLRG1(+) Th1 cells that persists poorly and can neither migrate into the lung parenchyma nor control Mtb growth. Furthermore, T-bet suppresses development of CD69(+)CD103(+) tissue resident phenotype effectors in lung. In contrast, Th1-cell-derived IFN-? inhibits the accumulation of intravascular CX3CR1(+)KLRG1(+) Th1 cells. Thus, although IL-12 and T-bet are essential host survival factors, they simultaneously oppose lung CD4 T cell responses at several levels, demonstrating the dual nature of Th1 polarization in tuberculosis. Published by Elsevier Inc.

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  2. DOI: 10.1016/j.celrep.2017.03.007
  3. PMID: 28355562

Library Notes

  1. Fiscal Year: FY2016-2017
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