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- W2020975034 endingPage "606" @default.
- W2020975034 startingPage "597" @default.
- W2020975034 abstract "The activation of immune-defense mechanisms in response to a microbial attack must be robust and appropriately tailored to fight particular types of pathogens. Infection with intracellular microorganisms elicits a type 1 inflammatory response characterized by mobilization of T helper type 1 (T(H)1) cells to the site of infection, where they are responsible for the recruitment and activation of macrophages. At the center of the type 1 inflammatory response is the transcription factor T-bet, a critical regulator of the T(H)1 differentiation program. T-bet induces the production of interferon-γ (IFN-γ) and orchestrates the T(H)1 cell-migratory program by regulating the expression of chemokines and chemokine receptors. However, tight regulation of the type 1 inflammatory response is essential for the prevention of immunopathology and the development of organ-specific autoimmunity. In this review, we discuss how T-bet expression drives autoaggressive and inflammatory processes and how its function in vivo must be delicately balanced to avoid disease." @default.
- W2020975034 created "2016-06-24" @default.
- W2020975034 creator A5006220266 @default.
- W2020975034 creator A5074049778 @default.
- W2020975034 date "2011-06-20" @default.
- W2020975034 modified "2023-10-07" @default.
- W2020975034 title "T-bet in disease" @default.
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