Metabolism controls CD4 T helper cell-induced pathogenicity during inflammatory bowel disease.

Despite medical advances, a significant proportion of inflammatory bowel disease (IBD) patients are resistant to therapies, with CD4 T cells being consistently activated. Analysis of inflamed tissues from a cohort of refractory IBD patients reveals an enrichment of metabolism gene transcripts in CD4 T cells. Exploring the mechanisms, our preliminary data demonstrate that several proinflammatory cytokines can independently trigger metabolic phenotypes which we believe reinvigorates the pathogenic function of CD4 T cells. This led us to formulate the hypothesis that IBD CD4 T cells, governed by metabolic cues, utilize common intracellular metabolites to drive inflammatory response that results in disease pathogenesis. Thus, our research goal is to identify the metabolic vulnerabilities of IBD CD4 T cells, which will consequently guide strategies for developing efficacious therapies.