Abstract
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.
© 2011 Pino-Lagos et al.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antineoplastic Agents / immunology
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Antineoplastic Agents / metabolism
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Antineoplastic Agents / pharmacology
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CD4-Positive T-Lymphocytes / immunology*
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CD4-Positive T-Lymphocytes / metabolism
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Cell Differentiation / drug effects
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Cell Differentiation / physiology*
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Cell Movement / drug effects
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Cell Movement / physiology*
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Graft Rejection / genetics
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Graft Rejection / immunology
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Graft Rejection / metabolism
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Immunity, Cellular / drug effects
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Immunity, Cellular / physiology*
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Immunization
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Inflammation / genetics
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Inflammation / immunology
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Inflammation / metabolism
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Mice
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Mice, Knockout
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Models, Immunological*
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Signal Transduction / drug effects
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Signal Transduction / physiology*
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Skin Transplantation / immunology
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Transplantation, Homologous
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Tretinoin / immunology*
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Tretinoin / metabolism
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Tretinoin / pharmacology
Substances
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Antineoplastic Agents
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Tretinoin