CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation.

ABSTRACT: Antigen-induced immune suppression, like T cell activation, requires antigen-presenting cells (APCs); however, the role of APCs in mediating these opposing effects is not well understood, especially in vivo. We report that genetic inactivation of CD11b, which is a CD18 subfamily of integrin receptors that is highly expressed on APCs, abolishes orally induced peripheral immune tolerance (oral tolerance) without compromising APC maturation or antigen-specific immune activation. The defective oral tolerance in CD11b(-/-) mice can be restored by adoptive transfer of wild-type APCs. CD11b deficiency leads to enhanced interleukin (IL) 6 production by APCs, which subsequently promotes preferential differentiation of naive T cells to T helper 17 (Th17) cells, which are a T cell lineage characteriz

SUBMITTER: Ehirchiou D 

PROVIDER: S-EPMC2118631 | biostudies-literature | 2007 Jul

REPOSITORIES: biostudies-literature