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Effect of long-term anti-CD4 or anti-CD8 treatment on the development of lpr CD4- CD8- double negative T cells and of the autoimmune syndrome in MRL-lpr/lpr mice
|Published in||Journal of Autoimmunity. 1995, vol. 8, no. 1, p. 33-45|
|Abstract||We have determined the effect of anti-CD4 or anti-CD8 monoclonal antibody (mAb) treatment from birth on the generation of the lpr CD4- CD8- double-negative (DN) T cell subset and on the development of lupus-like autoimmune syndrome in MRL-lpr/lpr mice. Both anti-CD4 and anti-CD8 mAb treatments resulted in a marked inhibition of lymph-adenopathy, whereas the development of the lpr DN T cells and of the lupus-like autoimmune syndrome strikingly differed in these two groups of mice. The treatment with anti-CD8 mAb almost completely blocked the appearance of the lpr DN T cells without any significant effect on the development of lupus-like autoimmune syndrome in MRL-lpr/lpr mice. In contrast, mice treated with anti-CD4 mAb failed to develop a lupus-like syndrome, while they still developed the lpr DN T cell subset, the predominant population in their lymph nodes, although absolute numbers were markedly diminished. Our results support the idea that CD8+ T cells are a major source of the lpr DN T cells, and that the lpr DN T cells play a minor, if any, role in the pathogenesis of lupus-like autoimmune syndrome in MRL-lpr/lpr mice.|
|Keywords||Animals — Antibodies, Monoclonal — Antigens, CD4/ immunology — Antigens, CD8/ immunology — Autoimmune Diseases/ immunology/pathology — Blotting, Northern — Cell Differentiation/immunology — Flow Cytometry — Lupus Erythematosus, Systemic/immunology — Lymph Nodes/pathology — Mice — Mice, Mutant Strains — T-Lymphocyte Subsets/ immunology|
|MERINO, Ramon et al. Effect of long-term anti-CD4 or anti-CD8 treatment on the development of lpr CD4- CD8- double negative T cells and of the autoimmune syndrome in MRL-lpr/lpr mice. In: Journal of Autoimmunity, 1995, vol. 8, n° 1, p. 33-45. doi: 10.1006/jaut.1995.0003 https://archive-ouverte.unige.ch/unige:11465|