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A retinoic acid–dependent checkpoint in the development of CD4(+) T cell–mediated immunity

It is known that vitamin A and its metabolite, retinoic acid (RA), are essential for host defense. However, the mechanisms for how RA controls inflammation are incompletely understood. The findings presented in this study show that RA signaling occurs concurrent with the development of inflammation....

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Detalles Bibliográficos
Autores principales: Pino-Lagos, Karina, Guo, Yanxia, Brown, Chrysothemis, Alexander, Matthew P., Elgueta, Raúl, Bennett, Kathryn A., De Vries, Victor, Nowak, Elizabeth, Blomhoff, Rune, Sockanathan, Shanthini, Chandraratna, Roshantha A., Dmitrovsky, Ethan, Noelle, Randolph J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171100/
https://www.ncbi.nlm.nih.gov/pubmed/21859847
http://dx.doi.org/10.1084/jem.20102358
Descripción
Sumario:It is known that vitamin A and its metabolite, retinoic acid (RA), are essential for host defense. However, the mechanisms for how RA controls inflammation are incompletely understood. The findings presented in this study show that RA signaling occurs concurrent with the development of inflammation. In models of vaccination and allogeneic graft rejection, whole body imaging reveals that RA signaling is temporally and spatially restricted to the site of inflammation. Conditional ablation of RA signaling in T cells significantly interferes with CD4(+) T cell effector function, migration, and polarity. These findings provide a new perspective of the role of RA as a mediator directly controlling CD4(+) T cell differentiation and immunity.