2026-08-25T15:21:17Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/271002025-12-20T01:18:19Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Cibrian, Danay author Saiz, María Laura author de la Fuente, Hortensia author Sánchez-Díaz, Raquel author Moreno-Gonzalo, Olga author Jorge, Inmaculada author Ferrarini, Alessia author Vázquez, Jesús author Punzón, Carmen author Fresno, Manuel author Vicente-Manzanares, Miguel author Daudén, Esteban author Fernández-Salguero, Pedro M author Martín, Pilar author Sánchez-Madrid, Francisco author 2016-08 The activation marker CD69 is expressed by skin γδ T cells. Here we found that CD69 controlled the aryl hydrocarbon receptor (AhR)-dependent secretion of interleukin 22 (IL-22) by γδ T cells, which contributed to the development of psoriasis induced by IL-23. CD69 associated with the aromatic-amino-acid-transporter complex LAT1-CD98 and regulated its surface expression and uptake of L-tryptophan (L-Trp) and the intracellular quantity of L-Trp-derived activators of AhR. In vivo administration of L-Trp, an inhibitor of AhR or IL-22 abrogated the differences between CD69-deficient mice and wild-type mice in skin inflammation. We also observed LAT1-mediated regulation of AhR activation and IL-22 secretion in circulating Vγ9(+) γδ T cells of psoriatic patients. Thus, CD69 serves as a key mediator of the pathogenesis of psoriasis by controlling LAT1-CD98-mediated metabolic cues. Nat Immunol. 2016 Aug;17(8):985-96. Nature Immunology 27376471 https://hdl.handle.net/20.500.12105/27100 CD69 controls the uptake of L-tryptophan through LAT1-CD98 and AhR-dependent secretion of IL-22 in psoriasis.