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- W2273094335 abstract "Calcitonin gene-related peptide (CGRP) is a neuropeptide with well-established immunomodulatory functions. CGRP-containing nerves innervate dermal blood vessels and lymph nodes. We examined whether CGRP regulates the outcome of Ag presentation by Langerhans cells (LCs) to T cells through actions on microvascular endothelial cells (ECs). Exposure of primary murine dermal microvascular ECs (pDMECs) to CGRP followed by coculture with LCs, responsive CD4(+) T cells and Ag resulted in increased production of IL-6 and IL-17A accompanied by inhibition of IFN-γ, IL-4, and IL-22 compared with wells containing pDMECs treated with medium alone. Physical contact between ECs and LCs or T cells was not required for this effect and, except for IL-4, we demonstrated that IL-6 production by CGRP-treated pDMECs was involved in these effects. CD4(+) cells expressing cytoplasmic IL-17A were increased, whereas cells expressing cytoplasmic IFN-γ or IL-4 were decreased by the presence of CGRP-treated pDMECs. In addition, the level of retinoic acid receptor-related orphan receptor γt mRNA was significantly increased, whereas T-bet and GATA3 expression was inhibited. Immunization at the site of intradermally administered CGRP led to a similar bias in CD4(+) T cells from draining lymph node cells toward IL-17A and away from IFN-γ. Actions of nerve-derived CGRP on ECs may have important regulatory effects on the outcome of Ag presentation with consequences for the expression of inflammatory skin disorders involving Th17 cells." @default.
- W2273094335 created "2016-06-24" @default.
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- W2273094335 date "2016-03-01" @default.
- W2273094335 modified "2023-10-16" @default.
- W2273094335 title "Calcitonin Gene–Related Peptide–Exposed Endothelial Cells Bias Antigen Presentation to CD4+ T Cells toward a Th17 Response" @default.
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- W2273094335 doi "https://doi.org/10.4049/jimmunol.1500303" @default.
- W2273094335 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4761517" @default.
- W2273094335 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26829986" @default.
- W2273094335 hasPublicationYear "2016" @default.
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