These results, along with the data from the IBD model, strongly suggest that the Tc17 differentiation program is cell-intrinsic, and that it is regulated differently among the CD8+ TN subsets, rendering the CD5lo subset the most skewed toward a highly pathogenic IL-17 producer, presumably in a wide range of acute and/or chronic inflammatory disease contexts. The gene discussed is IL17A; the disease is inflammatory bowel disease.