Carbon monoxide-treated dendritic cells decrease β1-integrin induction on CD8⁺ T cells and protect from type 1 diabetes.

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.

journal_name

Eur J Immunol

authors

Simon T,Pogu S,Tardif V,Rigaud K,Rémy S,Piaggio E,Bach JM,Anegon I,Blancou P

doi

10.1002/eji.201242684

subject

Has Abstract

pub_date

2013-01-01 00:00:00

pages

209-18

issue

1

eissn

0014-2980

issn

1521-4141

journal_volume

43

pub_type

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