Fossati L, Merino R, Iwamoto M, Lemoine R, Izui S
Department of Pathology, Centre Médical Universitaire, University of Geneva, Switzerland.
Eur J Immunol. 1994 Jul;24(7):1717-20. doi: 10.1002/eji.1830240741.
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.
为了评估Vβ8 + T细胞在MRL-lpr/lpr小鼠狼疮样自身免疫综合征发展中的作用，我们从出生到4个月龄用F23.1抗Vβ8单克隆抗体（mAb）对它们进行治疗。在此我们报告，F23.1 mAb治疗几乎完全耗尽Vβ8 + T细胞，既未抑制也未延迟MRL-lpr/lpr小鼠高球蛋白血症、自身抗体产生和自身免疫性肾小球肾炎的发展。此外，F23.1 mAb治疗并未阻止淋巴结病的发展以及CD4-CD8-双阴性T细胞亚群的产生，该亚群特征性地在lpr淋巴结中积聚。我们的结果强烈反对Vβ8 + T细胞在MRL-lpr/lpr小鼠狼疮样自身免疫综合征发展中起关键作用这一观点。
