Journal
JOURNAL OF IMMUNOLOGY
Volume 200, Issue 5, Pages 1543-1553Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1701618
Keywords
-
Categories
Funding
- National Institutes of Health [GM113961, AI119160, AI114543, GM115462, 5 T32 AI007485, 5 T32 CA009138]
- U.S. Department of Veterans Affairs Merit Review Award
- NATIONAL CANCER INSTITUTE [P30CA086862, T32CA009138] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI114543, R01AI083286, T32AI007485, R21AI119160, T32AI007511] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM115462, R01GM113961] Funding Source: NIH RePORTER
- Veterans Affairs [I01BX001324] Funding Source: NIH RePORTER
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available