Regulatory T cells (Treg) expressing the transcription factor Foxp3 are T cells which, in healthy individuals, keep CD4+ T cells in check. In patients with autoimmune diseases, Tregs are not as effective as in healthy individuals, and CD4+ T cells have an effector/memory phenotype and produce cytokines such as IFN-g, IL-17 and GM-CSF. Although the mechanisms by which Tregs control naïve CD4+ T cells have been well described, the mechanisms by which Tregs control effector/memory Th1, Th17 cells is not well understood.
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. Ongoing research in the laboratory focus on determining the mechanisms by which Tregs can control efficiently and specifically effector/memory T cells producing IFN-g, IL-17 or GM-CSF and how these effector/memory T cells can themselves impact Treg functions.
Additional Research Projects
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.
Modulation of the Immune Response by STAT1
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.
