RT Journal Article SR Electronic T1 CD69: An Unexpected Regulator of TH17 Cell–Driven Inflammatory Responses JF Science Signaling JO Sci. Signal. FD American Association for the Advancement of Science SP pe14 OP pe14 DO 10.1126/scisignal.2001825 VO 4 IS 165 A1 Martín, Pilar A1 Sánchez-Madrid, Francisco YR 2011 UL http://stke.sciencemag.org/content/4/165/pe14.abstract AB Mice lacking the C-type lectin receptor CD69 develop exacerbated forms of arthritis, contact dermatitis, allergic asthma, and autoimmune myocarditis. Because the immune responses in these diseases are largely mediated by a balance between proinflammatory subsets of T effector cells called T helper (TH) 17 cells and regulatory T cells, these findings indicate a previously unappreciated regulatory role for CD69 in modulating T lymphocyte differentiation toward the TH17 lineage and suggest a role in regulatory T cell function. CD69 promotes activation of the Jak3−signal transducer and activator of transcription 5 (Stat5) signaling pathway, which inhibits TH17 cell differentiation, thus providing a mechanistic link between CD69 and the regulation of TH17 responses. This evidence underscores the potential of CD69 as target in the treatment of autoimmune and allergic diseases and is consistent with mounting evidence linking CD69 to regulatory T cell subsets.