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- W1508779235 endingPage "134" @default.
- W1508779235 startingPage "119" @default.
- W1508779235 abstract "TNF-Α (TNF) is a pleiotropic cytokine which can have proinflammatory or immunosuppressive effects, depending on the context, duration of exposure and disease state. The basis for the opposing actions of TNF remains elusive. The growing appreciation of CD4+FoxP3+ regulatory T cells (Tregs), which comprise ∼10% of peripheral CD4 cells, as pivotal regulators of immune responses has provided a new framework to define the cellular and molecular basis underlying the contrasting action of TNF. TNF by itself can overcome the profound anergic state of T cell receptor-stimulated Tregs. Furthermore, in concert with IL-2, TNF selectively activates Tregs, resulting in proliferation, upregulation of FoxP3 expression and increases in their suppressive activity. Both human and mouse Tregs predominantly express TNFR2, making it possible for TNF to enhance Treg activity, which helps limit the collateral damage caused by excessive immune responses and eventually terminates immune response. TNFR2-expressing CD4+FoxP3+ Tregs comprise ∼40% of peripheral Tregs in normal mice and present the maximally suppressive subset of Tregs. In this review, studies describing the action of TNF on Treg function will be discussed. The role of Tregs in the autoimmune disorders and cancer as well as the effect of anti-TNF therapy on Tregs, especially in rheumatoid arthritis, will also be considered." @default.
- W1508779235 created "2016-06-24" @default.
- W1508779235 creator A5042240287 @default.
- W1508779235 creator A5059944329 @default.
- W1508779235 date "2010-01-01" @default.
- W1508779235 modified "2023-10-18" @default.
- W1508779235 title "TNF-α: An Activator of CD4+FoxP3+TNFR2+ Regulatory T Cells" @default.
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- W1508779235 doi "https://doi.org/10.1159/000289201" @default.