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• W2943117968 abstract "Recent seminal studies have revealed that laboratory mice differ from adult humans with regard to the frequency, number, and distribution of memory T cells. Because our data show that memory T cells are more susceptible to sepsis-induced death than naive T cells, in this study we developed a model in which mice possess a memory T cell compartment more similar to that of adult humans, to better study immune responses during sepsis in the more physiologically relevant context of high frequencies of memory T cells. Using this model, we found that CD44hi memory T cells significantly upregulated the coinhibitory molecule 2B4 during sepsis, and 2B4+ memory T cells coexpressed markers of both activation and exhaustion. Genetic deficiency in 2B4 resulted in decreased mortality during sepsis. Mechanistically, this decreased mortality was associated with reduced caspase-3/7+ apoptotic T cells in 2B4–/– relative to WT, septic hosts. These results were corroborated by analysis of PBMCs isolated from human patients with sepsis, which showed increased frequencies of caspase-3/7+ apoptotic cells among 2B4+ relative to 2B4– T cells. Thus, 2B4 plays a critical role in sepsis-induced apoptosis in both murine memory T cells and those isolated from human patients with sepsis." @default.
• W2943117968 created "2019-05-09" @default.
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• W2943117968 date "2019-05-02" @default.
• W2943117968 modified "2023-10-15" @default.
• W2943117968 title "Increased attrition of memory T cells during sepsis requires 2B4" @default.
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• W2943117968 doi "https://doi.org/10.1172/jci.insight.126030" @default.
• W2943117968 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6538360" @default.
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• W2943117968 hasPublicationYear "2019" @default.
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