Role of CD5+ B-1 cells in EAE pathogenesis.
Hybridoma cell lines producing natural autoantibodies (NAA), generated from A.SW mice with progressive experimental autoimmune encephalomyelitis (P-EAE), have been shown to cause demyelination and renal pathology when injected into naive mice. To investigate the relative contribution of these antibodies to disease pathogenesis, B-1 cells, the major producers of NAA, were depleted by hypotonic shock. Depletion of B-1 cells during the effector phase of EAE significantly decreased the severity of demyelination and overall pathology in the brain. There was also a decreased incidence of P-EAE and a decrease in clinical score. Depletion during the induction phase of the disease resulted in an increase in the incidence of P-EAE and in the clinical score. Overall, B-1 cells were found to modulate EAE pathogenesis.
Peterson
Lisa K
LK
Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.
Tsunoda
Ikuo
I
Fujinami
Robert S
RS
D000818:Animals; D001323:Autoantibodies / Q000276:immunology*; D016175:B-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology; D001921:Brain / Q000473:pathology; D018956:CD5 Antigens / Q000276:immunology*; D049109:Cell Proliferation; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D051379:Mice; D008811:Mice, Inbred DBA; D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein / Q000276:immunology; D063308:Myelin-Oligodendrocyte Glycoprotein; D010529:Peritoneal Cavity / Q000166:cytology; D013997:Time Factors
D001323:Autoantibodies; D018956:CD5 Antigens; C571327:Mog protein, mouse; D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein; D063308:Myelin-Oligodendrocyte Glycoprotein