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• W2116795083 abstract "This study affirmed that isolated CD8(+) T cells express mRNA and produce TGF-β following cognate peptide recognition. Blockage of endogenous TGF-β with either a TGF-β-blocking Ab or a small molecule inhibitor of TGF-βRI enhances the generation of CD62L(high)/CD44(high) central memory CD8(+) T cells accompanied with a robust recall response. Interestingly, the augmentation within the central memory T cell pool occurs in lieu of cellular proliferation or activation, but with the expected increase in the ratio of the Eomesoderm/T-bet transcriptional factors. Yet, the signal transduction pathway(s) seems to be noncanonical, independent of SMAD or mammalian target of rapamycin signaling. Enhancement of central memory generation by TGF-β blockade is also confirmed in human PBMCs. The findings underscore the role(s) that autocrine TGF-β plays in T cell homeostasis and, in particular, the balance of effector/memory and central/memory T cells. These results may provide a rationale to targeting TGF-β signaling to enhance Ag-specific CD8(+) T cell memory against a lethal infection or cancer." @default.
• W2116795083 created "2016-06-24" @default.
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• W2116795083 date "2013-07-31" @default.
• W2116795083 modified "2023-10-15" @default.
• W2116795083 title "Inhibition of TGF-β1 Signaling Promotes Central Memory T Cell Differentiation" @default.
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• W2116795083 doi "https://doi.org/10.4049/jimmunol.1300472" @default.
• W2116795083 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3889640" @default.
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