LACK OF ASSOCIATION OF V-BETA-8(-CELLS WITH LUPUS-LIKE SYNDROME IN MRL-LPR() T)LPR MICE/

To evaluate the role of V beta 8(+) T cells in the development of lupu s-like autoimmune syndrome in MRL-lpr/lpr mice, we treated them with t he F23.1 anti-V beta 8 monoclonal antibody (mAb) from birth to 4 month s of age. Here we report that almost complete depletion of V beta 8(+) T cells by the F23.1 mAb treatment neither inhibited nor delayed the development of hypergammaglobulinemia, autoantibody production and aut oimmune glomerulonephritis in MRL-lpr/lpr mice. In addition, the F23.1 mAb treatment did not prevent the development of lymphadenopathy and the generation of a CD4(-) CD8(-) double-negative T cell subset, chara cteristically accumulating in lpr lymph nodes. Our results strongly ar gue against the idea that the V beta 8(+) T cells play a critical role in the development of lupus-like autoimmune syndrome in MRL-lpr/lpr m ice.