Lack of association of V beta 8+ T cells with lupus-like syndrome in MRL-lpr/lpr mice.
To evaluate the role of V beta 8+ T cells in the development of lupus-like autoimmune syndrome in MRL-lpr/lpr mice, we treated them with the F23.1 anti-V beta 8 monoclonal antibody (mAb) from birth to 4 months 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 autoimmune 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, characteristically accumulating in lpr lymph nodes. Our results strongly argue 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 mice.
Department of Pathology, Centre Médical Universitaire, University of Geneva, Switzerland.
L
L
Fossati
R
R
Merino
M
M
Iwamoto
R
R
Lemoine
S
S
Izui
D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000954:Antigens, Surface / Q000096:biosynthesis; D004195:Disease Models, Animal; D005434:Flow Cytometry; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000517:prevention & control; D008206:Lymphatic Diseases / Q000276:immunology* / Q000517:prevention & control; D051379:Mice; D008817:Mice, Mutant Strains; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*
D000911:Antibodies, Monoclonal; D000954:Antigens, Surface; D016693:Receptors, Antigen, T-Cell, alpha-beta