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Sci. Signal., 22 March 2011
Vol. 4, Issue 165, p. pe14
[DOI: 10.1126/scisignal.2001825]

PERSPECTIVES

CD69: An Unexpected Regulator of TH17 Cell–Driven Inflammatory Responses

Pilar Martín1* and Francisco Sánchez-Madrid1,2*

1 Department of Vascular Biology and Inflammation, Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.
2 Servicio de Inmunología, Hospital de La Princesa, Universidad Autónoma de Madrid, 28006 Madrid, Spain.

Abstract: 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.

* Corresponding authors. E-mail, pmartinf{at}cnic.es (P.M.); fsanchez.hlpr{at}salud.madrid.org (F.S.-M.)

Citation: P. Martín, F. Sánchez-Madrid, CD69: An Unexpected Regulator of TH17 Cell–Driven Inflammatory Responses. Sci. Signal. 4, pe14 (2011).

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