ASC controls T-bet-dependent CTL differentiation and defines transplant outcome independent of the inflammasome

ABSTRACT: The adaptor protein ASC is known to facilitate caspase-1 activation essential for innate host immunity via the formation of the inflammasome complex - a multi-protein structure responsible for processing IL-1beta and IL-18 to their active moieties. Here we demonstrate that ASC-deficient CD8+ T cells fail to induce graft-versus-host disease (GVHD) and have impaired capacity for graft rejection and graft-versus-leukemia (GVL) activity. These effects are the result of an inability to differentiate into fully cytolytic, granzyme B-expressing effector cells, with a developmental bias instead towards CD127+KLRG1- memory CD8+ T cells. These alterations in differentiation are inflammasome-independent, since GVHD lethality and CTL differentiation are not altered in recipients of caspase-1-deficien

ORGANISM(S): Mus musculus

SUBMITTER: Glen Boyle 

PROVIDER: E-GEOD-78755 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress