| First Author | Ehirchiou D | Year | 2007 |
| Journal | J Exp Med | Volume | 204 |
| Issue | 7 | Pages | 1519-24 |
| PubMed ID | 17562817 | Mgi Jnum | J:125874 |
| Mgi Id | MGI:3760062 | Doi | 10.1084/jem.20062292 |
| Citation | Ehirchiou D, et al. (2007) CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation. J Exp Med 204(7):1519-24 |
| abstractText | 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 characterized by their production of IL-17. Consequently, antigen feeding and immunization of CD11b(-/-) mice results in significant production of IL-17 within the draining lymph nodes that interferes with the establishment of oral tolerance. Together, we conclude that CD11b facilitates oral tolerance by suppressing Th17 immune differentiation. |
