Commensurate with ex vivo and in vitro phenotypes upon miR-34a manipulation, deficiency of miR-34a in antigen-presenting cells resulted in the lack of development of antigen-specific Th17 cells, confirmed by low serum concentrations of IL-17; and an attenuated joint pathology in miR-34a−/− mice during experimental arthritis. This evidence concerns the gene IL17A and Arthritis.