Betsy J. Barnes

Abstract Diamond Blackfan anemia syndrome (DBAS) is a congenital ribosomopathy caused by haploinsufficiency of ribosomal proteins (RPs), but how RP stoichiometry and activity regulates erythroid development remains enigmatic. Using in vivo models, we uncover divergent functions for the small and large ribosomal subunit proteins RPS19 and RPL5 in fetal hematopoiesis.

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Highlights • IRF5 in CD4+ T cells promotes Th1- and Th17- and decreases Th2-associated cytokines • IRF5 in CD4+ T cells promotes chemokine receptor-initiated signaling and expression • T cell-intrinsic IRF5 increases the severity of experimental colitis in mice • IRF5 disease-risk variant human CD4+ T cells demonstrate altered T cell outcomes Summary IRF5 polymorphisms are associated with multiple immune-mediated diseases, including ulcerative colitis.