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Sepsis-Induced T Cell Immunoparalysis: The Ins and Outs of Impaired T Cell Immunity

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JOURNAL OF IMMUNOLOGY
卷 200, 期 5, 页码 1543-1553

出版社

AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1701618

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资金

  1. National Institutes of Health [GM113961, AI119160, AI114543, GM115462, 5 T32 AI007485, 5 T32 CA009138]
  2. U.S. Department of Veterans Affairs Merit Review Award
  3. NATIONAL CANCER INSTITUTE [P30CA086862, T32CA009138] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI114543, R01AI083286, T32AI007485, R21AI119160, T32AI007511] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM115462, R01GM113961] Funding Source: NIH RePORTER
  6. Veterans Affairs [I01BX001324] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Sepsis results in a deluge of pro- and anti-inflammatory cytokines, leading to lymphopenia and chronic immunoparalysis. Sepsis-induced long-lasting immunoparalysis is defined, in part, by impaired CD4 and CD8 ab T cell responses in the postseptic environment. The dysfunction in T cell immunity affects naive, effector, and memory T cells and is not restricted to classical ab T cells. Although sepsis-induced severe and transient lymphopenia is a contributory factor to diminished T cell immunity, T cell-intrinsic and -extrinsic factors/ mechanisms also contribute to impaired T cell function. In this review, we summarize the current knowledge of how sepsis quantitatively and qualitatively impairs CD4 and CD8 T cell immunity of classical and nonclassical T cell subsets and discuss current therapeutic approaches being developed to boost the recovery of T cell immunity postsepsis induction.

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