| First Author | Inoue A | Year | 1997 |
| Journal | Int Immunol | Volume | 9 |
| Issue | 12 | Pages | 1837-47 |
| PubMed ID | 9466311 | Mgi Jnum | J:45032 |
| Mgi Id | MGI:1101646 | Doi | 10.1093/intimm/9.12.1837 |
| Citation | Inoue A, et al. (1997) Anti-adhesion molecule therapy in Theiler's murine encephalomyelitis virus-induced demyelinating disease. Int Immunol 9(12):1837-47 |
| abstractText | We examined the role of leukocyte function-associated antigen (LFA)-1 and its counter-receptor intercellular adhesion molecule (ICAM)-1, one of the most important pairs of adhesion molecules, in the development of Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD). Immunohistochemical study showed hyper-expression of ICAM-1 on vascular endothelial cells and expression of LFA-1 on mononuclear infiltrating cells in the spinal cords of TMEV-infected mice. Treatment with mAb to ICAM-1 and/or LFA-1 molecules resulted in significant suppression of the development of demyelinating disease, both clinically and histologically, with down-regulation in the CNS of the respective adhesion molecules after treatment. In mice treated with these mAb, the specific delayed-type hypersensitivity and T cell proliferative responses for TMEV were decreased. The production of tumor necrosis factor-alpha and IFN-gamma in spleen cells was also decreased, but IL-4 production remained unchanged. These data suggest that ICAM-1/LFA-1 interaction is critically involved in the pathogenesis of TMEV-IDD and that antibodies to these adhesion molecules could be a novel therapeutic approach to the treatment of demyelinating diseases such as human multiple sclerosis. |
