Several microRNAs are known to affect the function and development of lymphocytes and to modulate autoimmune pathogenesis. In Nature Medicine, Zhu et al. show that expression of the microRNA miR-23b is downregulated at local sites of inflammation in patients with rheumatoid arthritis or systemic lupus erythematosus and in the corresponding mouse models and that this contributes to enhanced pathogenesis. IL-17 suppresses the transcription of miR-23b, partially through the recruitment of the regulatory factors NF-κB and IκBζ to the promoter of miR-23b. This microRNA suppresses tumor necrosis factor–, IL-1β- and IL-17-mediated activation of NF-κB by targeting the expression of TAB2 and TAB3, two essential signaling mediators downstream of those proinflammatory cytokines. The expression of miR-23b in nonhematopoietic, radioresistant cells is protective in mouse models of rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis, which suggests that miR-23b functions as a local anti-inflammatory modulator in many autoimmune diseases.

Nat. Med. (3 June 2012) doi:10.1038/nm.2815