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• W1532375382 abstract "Carbon monoxide (CO) treatment improves pathogenic outcome of autoimmune diseases by promoting tolerance. However, the mechanism behind this protective tolerance is not yet defined. Here, we show in a transgenic mouse model for autoimmune diabetes that ex vivo gaseous CO (gCO)-treated DCs loaded with pancreatic β-cell peptides protect mice from disease. This protection is peptide-restricted, independent of IL-10 secretion by DCs and of CD4(+) T cells. Although no differences were observed in autoreactive CD8(+) T-cell function from gCO-treated versus untreated DC-immunized groups, gCO-treated DCs strongly inhibited accumulation of autoreactive CD8(+) T cells in the pancreas. Interestingly, induction of β1-integrin was curtailed when CD8(+) T cells were primed with gCO-treated DCs, and the capacity of these CD8(+) T cells to lyse isolated islet was dramatically impaired. Thus, immunotherapy using CO-treated DCs appears to be an original strategy to control autoimmune disease." @default.
• W1532375382 created "2016-06-24" @default.
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• W1532375382 date "2012-12-11" @default.
• W1532375382 modified "2023-10-17" @default.
• W1532375382 title "Carbon monoxide-treated dendritic cells decrease β1-integrin induction on CD8⁺T cells and protect from type 1 diabetes" @default.
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• W1532375382 doi "https://doi.org/10.1002/eji.201242684" @default.
• W1532375382 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23065740" @default.
• W1532375382 hasPublicationYear "2012" @default.
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