Signal transducer and activator of transcription 1 (STAT1) is a transcription factor activated by type I and II interferons. This response needs to be fine-tuned because diminished or excessive STAT1-mediated signaling leads to enhanced susceptibility to viral, bacterial, and fungal infections and the development of autoimmune diseases.
Using loss and gain of function models, the Bettelli Lab is currently investigating how STAT1-mediated signaling modulates the function of different immune cells and participates in the pathogenesis of different autoimmune diseases.
Additional Research Projects
Discover more research projects from the
Bettelli Lab.
Control of the Immune Response by DOCK8
The lab has been studying the mechanisms by which DOCK8 modulates the function of adaptive and innate cells and contributes to the progression of autoimmunity.
Mechanisms of T Cell Differentiation and Pathogenicity
T cells differentiate in different subsets of effector T helper (Th) cells and have specialized effector functions.
Mechanisms of T Cell Regulation
The Bettelli Lab has discovered that Th cells producing IFN-g, IL-17 and GM-CSF are differentially regulated by Tregs during the course of central nervous system (CNS) autoimmunity.
