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- W59337153 abstract "Alpha-MSH is a potent anti-inflammatory neuropeptide. We previously reported our discovery that mouse CD4+ T cells primed to function as Th1 cells are suppressed in their expected Th1 functionality when treated with α-MSH as they were restimulated through their T cell receptor (Tcr). Also, we discovered that the re-stimulated α-MSH-treated primed CD4+ T cells are now TGF-β-producing CD25+ Treg cells. We asked whether these α-MSH-induced Treg cells express markers and FoxP3 in common with other characterized Treg cells. In addition, we examined the possibility that α-MSH expands the natural CD25+ Treg cells in the primed CD4+ T cell population. The α-MSH-treated Tcr-stimulated primed CD25+ CD4+ T cells had high expression of CD44 and CTLA-4, and low expression of CD62L and GITR. The FoxP3 mRNA levels in the CD4+ T cells were 2-fold enhanced by α-MSH-treatment with a parallel decline in high CD127 expression. The depletion of CD25+ cells from the primed CD4+ T cell population before restimulation prevented activation of Th1 cell functionality, but did not change α-MSH-induced TGF-β production. Therefore, α-MSH-induces Treg cells that are found in the CD25+ CD4+ T cell population that are not derived from natural CD25+ CD4+ Treg cells. The results suggest that α-MSH is a potential Treg cell differentiation factor with implications on α-MSH activity at the resolution of immune responses and in immune homeostasis. Work supported by PHS grant EY10752" @default.
- W59337153 created "2016-06-24" @default.
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- W59337153 date "2008-03-01" @default.
- W59337153 modified "2023-10-14" @default.
- W59337153 title "Alpha‐melanocyte stimulating hormone (α‐MSH) induction of Treg cell differentiation" @default.
- W59337153 doi "https://doi.org/10.1096/fasebj.22.1_supplement.661.21" @default.
- W59337153 hasPublicationYear "2008" @default.
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