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- W1982323892 abstract "In humans, DOCK8 immunodeficiency syndrome is characterized by severe cutaneous viral infections. Thus, CD8 T cell function may be compromised in the absence of DOCK8. In this study, by analyzing mutant mice and humans, we demonstrate a critical, intrinsic role for DOCK8 in peripheral CD8 T cell survival and function. DOCK8 mutation selectively diminished the abundance of circulating naive CD8 T cells in both species, and in DOCK8-deficient humans, most CD8 T cells displayed an exhausted CD45RA+CCR7− phenotype. Analyses in mice revealed the CD8 T cell abnormalities to be cell autonomous and primarily postthymic. DOCK8 mutant naive CD8 T cells had a shorter lifespan and, upon encounter with antigen on dendritic cells, exhibited poor LFA-1 synaptic polarization and a delay in the first cell division. Although DOCK8 mutant T cells underwent near-normal primary clonal expansion after primary infection with recombinant influenza virus in vivo, they showed greatly reduced memory cell persistence and recall. These findings highlight a key role for DOCK8 in the survival and function of human and mouse CD8 T cells." @default.
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- W1982323892 date "2011-10-17" @default.
- W1982323892 modified "2023-10-16" @default.
- W1982323892 title "DOCK8 deficiency impairs CD8 T cell survival and function in humans and mice" @default.
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- W1982323892 doi "https://doi.org/10.1084/jem.20110345" @default.
- W1982323892 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3201196" @default.
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