INTERPLAY BETWEEN CONVENTIONAL AND NON-CONVENTIONAL T CELLS IN INFLAMMATORY BOWEL DISEASE

<p dir="ltr">Inflammatory bowel disease (IBD) is a spectrum of disorders characterized by distinct patterns of intestinal inflammation and a dysregulated intestinal immune response. Given the growing number of new diagnoses and the inconsistent results of current treatments, there is a major unmet need to understand IBD pathology to develop more effective therapies. The IBD-associated immune response is highly multi-faceted and consists of a network of adaptive CD4 T cells and innate-like γδ T cells that both produce inflammatory cytokines and are associated with enhanced intestinal damage. Despite the association of these cell types with IBD pathogenesis, how these responses become dysregulated and contribute to intestinal pathology remains largely undefined. Here, I demonstrate that mice with CD4 T cell-specific deletions in the transcription factors STAT3 and BATF develop spontaneous colitis marked by elevated numbers of inflammatory γδ T cells that mimic those found in human IBD. Together, these data indicate that a STAT3/BATF-sufficient CD4 T cell population is critical for regulation of inflammatory γδ T cells and that therapeutic targeting of this adaptive/innate-like T cell interaction may be beneficial in preventing or treating IBD.</p>