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- W9652024 abstract "Abstract Calcineurin (CN), a protein phosphatase activated by Ca2+-calmodulin, is involved in activation of NFAT by its dephosphorylation. CN inhibitors such as cyclosporine A (CsA) and FK506 are potent inhibitors of T-cell responses and are commonly used to prevent graft rejection. Consistently, CNAβ-deficient mice exhibit defective thymocyte maturation in young mice. However, T cells undergo spontaneous activation in older Cnab-/- mice, which develop splenomegaly, thymomegaly, hepatomegaly and succumb to metastatic B-cell lymphomas. We have also observed that FOXP3+ Treg cells are decreased while mature activated CD4+ and CD8+ T cells (CD62L-CD44+) are increased in Cnab-/- mice compared to age-matched control mice. These data show that CNAβ is important for the development and homeostasis of mature T cells and Treg cells. Cytokine profile analysis revealed that CNAβ signaling is required to inhibit proinflammatory cytokines (IL-4, IL-10, IL-17 and IFNγ) by TGFβ1 and TGFβ1 induced FOXP3 expression in T cells, suggesting that CNAβ signaling is required for Treg-cell generation. The data suggest that in the absence of CNAβ, a defective T-cell regulatory environment leads to accumulation of activated T cells which produce proinflammatory cytokines and cause inflammation and cancer. Grant support: This study was supported by NIH AI067903 and CA84291 to TD, and IRG7400128 to RB." @default.
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- W9652024 date "2009-04-01" @default.
- W9652024 modified "2023-10-16" @default.
- W9652024 title "Calcineurin Ab deficiency causes defective Treg-cell generation and enhanced effector T-cell differentiation (89.13)" @default.
- W9652024 doi "https://doi.org/10.4049/jimmunol.182.supp.89.13" @default.
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