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

First Author  Wang Y Year  2007
Journal  Biochem Biophys Res Commun Volume  353
Issue  4 Pages  857-62
PubMed ID  17207459 Mgi Jnum  J:117845
Mgi Id  MGI:3697797 Doi  10.1016/j.bbrc.2006.12.104
Citation  Wang Y, et al. (2007) A critical role of LFA-1 in the development of Th17 cells and induction of experimental autoimmune encephalomyelytis. Biochem Biophys Res Commun 353(4):857-62
abstractText  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 naive CD4(+) T cells to the dLN.
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