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- W4313374413 abstract "Abstract Immune responses to an infection are controlled by various factors including antigens, co-stimulatory molecules and cytokines present in the tissue micro-environment. TGFβ is a pleiotropic cytokine that modulates immune response and cellular differentiation usually through SMAD (Smad 2,3 & 4)-mediated signaling cascade. Interestingly, TGFβ and Smad4 have independent and opposing roles in determining the fate of activated CTLs. While TGFβ-receptor mediated signaling is required for resident memory (TRM) cells, Smad4 is required for effector (TEff) and central memory subsets (TCM). However, the mechanism behind TGFβ as well as Smad4 mediated differentiation is yet to be unraveled. Using transgenic animal models and pharmacological inhibitors, we investigate the role of TGFβ and multiple SMAD proteins in determining the fate of activated CTLs. We identified that while canonical TGFβ signaling, through Smad2 and Smad3, induces CD103 expression (TRM), Smad4 inhibits CD103 expression thus preventing TRM differentiation. In addition, targeted-ablation of Smad4 alters the expression of various transcription factors that participate in fate determination, including Eomes and KLF2. Although Eomes has previously been implicated in negative regulation of CD103, over-expression of Eomes does not affect CD103 expression in the absence of Smad4. This suggests that Smad4 is required for negative regulation of CD103. These results reveal a novel central role for Smad4 in guiding the fate decisions of activated CTLs and tissue localization via multiple intersecting signaling pathways." @default.
- W4313374413 created "2023-01-06" @default.
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- W4313374413 date "2020-05-01" @default.
- W4313374413 modified "2023-09-27" @default.
- W4313374413 title "Smad signaling determines the fate of activated CTLs via multiple intersecting signaling pathways" @default.
- W4313374413 doi "https://doi.org/10.4049/jimmunol.204.supp.77.17" @default.
- W4313374413 hasPublicationYear "2020" @default.
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