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- W2114049068 abstract "T-bet, a tissue-specific transcription factor, controls T helper 1 (Th1) cell differentiation and IFN-production. Given the reciprocal relationship between Th1 and other types of helper T cells, we hypothesized that T-bet impacts multiple helper and regulatory T (Treg) cells, thereby influencing the magnitude of autoimmune disease. We tested this hypothesis in an experimental model of autoimmune myasthenia gravis (EAMG) of mice. Myasthenia gravis (MG) and EAMG are T cell-driven, IgG autoantibody-mediated disorders that destroy muscles by attacking the target antigen acetylcholine receptor (AChR) or other antigens of skeletal muscle at neuromuscular junctions. We show that, compared to wild-type mice, AChR-primed T-bet-/- mice are less susceptible to EAMG. This phenotype is associated with a reduction of autoreactive Th1 cells and augmentation of Th2 and Th17 cells as well as an upregulation of Foxp3 expression by T-bet-/-CD4+CD25+ Treg cells. Thus, in our model, T-bet not only specifies the Th1 lineage but also has a broad influence on autoreactive Th2, Th17 and Treg cells. These coordinated effects reduce the genesis of pathogenic antibodies and protect against B cell-mediated EAMG." @default.
- W2114049068 created "2016-06-24" @default.
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- W2114049068 date "2009-12-01" @default.
- W2114049068 modified "2023-10-17" @default.
- W2114049068 title "T-bet deficiency decreases susceptibility to experimental myasthenia gravis" @default.
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- W2114049068 doi "https://doi.org/10.1016/j.expneurol.2009.09.022" @default.
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