Protection against experimental autoimmune encephalomyelitis requires both CD4+ T suppressor cells and myelin basic protein-primed B cells.
Suppressor cells that regulate experimental autoimmune encephalomyelitis (EAE) are present in rats that recover from the disease and can protect against the development of active EAE when transferred to normal recipients. Both CD4+ T suppressor cells, known to regulate EAE effector cell lymphokine production, and myelin basic protein (MBP)-primed B cells are required to transfer protection against EAE to normal recipients. Neither CD4+ T suppressor cells nor MBP-primed B cells alone could transfer protection. Moreover, the co-transfer of normal B cells with CD4+ T suppressor cells did not provide protection against EAE. These results suggest that the regulation of EAE and perhaps the recovery from acute clinical disease requires the interaction of two specific subpopulations of regulatory lymphocytes.
Karpus
W J
WJ
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201.
Swanborg
R H
RH
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology* / Q000637:transplantation; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000517:prevention & control*; D005260:Female; D007116:Immunization, Passive; D004676:Myelin Basic Protein / Q000276:immunology*; D051381:Rats; D011917:Rats, Inbred Lew; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000637:transplantation
D004676:Myelin Basic Protein