{Reference Type}: Journal Article
{Title}: Th2 cells lacking T-bet suppress naive and memory T cell responses via IL-10.
{Author}: Muñoz M;Hegazy AN;Brunner TM;Holecska V;Marek RM;Fröhlich A;Löhning M;
{Journal}: Proc Natl Acad Sci U S A
{Volume}: 118
{Issue}: 6
{Year}: 02 2021 9
{Factor}: 12.779
{DOI}: 10.1073/pnas.2002787118
{Abstract}: Exacerbated immune responses and loss of self-tolerance lead to the development of autoimmunity and immunopathology. Novel therapies to target autoreactive T cells are still needed. Here, we report that Th2-polarized T cells lacking the transcription factor T-bet harbor strong immunomodulatory potential and suppress antigen-specific CD8+ T cells via IL-10. Tbx21-/- Th2 cells protected mice against virus-induced type 1 diabetes development and suppressed not only naive but also memory CD8+ T cell responses. IL-10-producing, but not IL-10-deficient Tbx21-/- Th2 cells down-regulated costimulatory molecules on dendritic cells and reduced their IL-12 production after lymphocytic choriomeningitis virus infection. Impaired dendritic cell activation hindered effector and cytotoxic CD8+ T cell development after infection. These findings indicate that Tbx21-/- Th2 cells strongly suppress proinflammatory responses of naive and memory T cells via IL-10. Thus, in vivo IL-10-secreting Th2 cells could harbor a therapeutic potential for the treatment of T cell-mediated inflammatory disorders.