Augmentation of adoptively transferred experimental allergic encephalomyelitis by administration of a monoclonal antibody specific for LFA-1 alpha.
We investigated the effect of an anti-leukocyte function antigen 1 (LFA-1 alpha) monoclonal antibody, M17/4.2, on murine relapsing experimental allergic encephalomyelitis (EAE). In vitro investigations demonstrated that M17/4.2 inhibited proliferation with concanavalin A or myelin basic protein. Control mice treated with phosphate buffered saline (PBS) developed a mild to moderate disease at 7-10 days followed by a long-term relapsing clinical course. With administration of M17/4.2, the time of disease onset was unchanged; however, the severity of the disease was greatly augmented, resulting in early mortality. The pathology correlated well with the clinical course. M17/4.2 mice showed more inflammation and demyelination than PBS or anti-CD4 treated mice. Therefore, this anti-LFA-1 specific monoclonal antibody augmented EAE.
Welsh
C T
CT
Neurovirology Research Laboratory, VAMC, Salt Lake City, UT 84148.
Rose
J W
JW
Hill
K E
KE
Townsend
J J
JJ
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000473:pathology; D005260:Female; D006168:Guinea Pigs; D007116:Immunization, Passive; D016169:Lymphocyte Function-Associated Antigen-1 / Q000276:immunology*; D051379:Mice; D004676:Myelin Basic Protein / Q000276:immunology; D051381:Rats
D000911:Antibodies, Monoclonal; D016169:Lymphocyte Function-Associated Antigen-1; D004676:Myelin Basic Protein