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Biochem Biophys Res Commun. 2007 Feb 23;353(4):857-62. Epub 2006 Dec 22.

A critical role of LFA-1 in the development of Th17 cells and induction of experimental autoimmune encephalomyelytis.

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  • 1Department of Immunology, Institute of Basic Medical Sciences and Center for TARA, University of Tsukuba, 1-1-1 Ten-nodai, Tsukuba, Ibaraki 305-8575, Japan.

Abstract

The alphaLbeta2 integrin adhesion molecule LFA-1 is believed to be involved in the migration of autoreactive T cells to the central nervous system across the endothelial blood-brain barrier in experimental autoimmune encephalomyelitis (EAE). Here, we demonstrate that the incidence and clinical scores of EAE in LFA-1-/- mice induced by the immunization with the myelin oligodendrocyte glycoprotein (MOG)-peptide antigen were significantly lower than those in wild type mice. Further studies demonstrated that lymphocytes recruitment to the draining lymph nodes (dLN) after the immunization with the MOG-peptide was severely suppressed in LFA-1-/- mice. Moreover, generation of the MOG-specific IL-17-producing helper T (Th17) cells in the dLN was impaired in LFA-1-/- mice. These results suggest that LFA-1 may play an important role for the generation of MOG-specific Th17 cells in the dLN as well as the immigration of MOG-specific naïve CD4+ T cells to the dLN.

PMID:
17207459
[PubMed - indexed for MEDLINE]
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