Hyper-Ia antigen expression on B cells from B6-lpr/lpr mice correlates with manifestations of the autoimmune state.
To investigate the state of activation of B cells from mice with the lpr gene defect, membrane Ia antigen (mIa) expression was analyzed on B cells from B6-lpr/lpr (lpr) and control B6- +/-/+/- mice. B cells from lpr mice exhibited marked increases in levels of mIa as determined by flow cytometry using a monoclonal anti-I-Ab,d reagent. This increase, which was progressive with age, suggests that phenotypic alteration of B-cell mIa expression is a consequence of lpr gene action. Since B-cell activation manifest by elevated mIa expression may promote productive interactions with helper T cells, these observations suggest an important role for B-cell abnormalities in the etiology of lpr-induced autoimmune disease.
D000818:Animals; D001323:Autoantibodies / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000276:immunology*; D051379:Mice; D008817:Mice, Mutant Strains / Q000276:immunology*; D010641:Phenotype
D001323:Autoantibodies; D000949:Histocompatibility Antigens Class II