Tissue-resident memory T cells break tolerance to renal autoantigens and orchestrate immune-mediated nephritis.

ABSTRACT: Immune-mediated nephritis is a leading cause of acute kidney injury and chronic kidney disease. While the role of B cells and antibodies has been extensively investigated in the past, the advent of immune-checkpoint inhibitors has led to a reappraisal of the role of T cells in renal immunology. However, it remains elusive how T cells with specificity for renal autoantigens are activated and participate in immune-mediated nephritis. Here, we followed the fate and function of pathogen-activated autoreactive CD8 T cells that are specific for a renal autoantigen. We demonstrate that recently activated splenic CD8 T cells developed a hybrid phenotype in the context of renal autoantigen cross-presentation, combining hallmarks of activation and T cell dysfunction. While circulating memory T cells

SUBMITTER: Arnold F 

PROVIDER: S-EPMC11364874 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature