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患自发性自身免疫病的小鼠(MLR- 1pr/1pr和(NZB×NZW)F1小鼠],其有丝分裂因子诱导的IL2生成以及细胞增生作用均有严重缺损。这种缺损包括:生成IL2的T细胞对ConA加IL 1的作用不产生反响和反应性T细胞对ConA的作用不敏感,从而使这些细胞不能对IL 2产生增生反应。对这一功能异常的分子学基础尚不甚了解。推
Mice with spontaneous autoimmune disease (MLR-1pr / 1pr and (NZB × NZW) F1 mice) had severe defects in both mitogenic factor-induced IL2 production and cell proliferation, including defects in the production of IL2 T cells do not respond to ConA plus IL 1 and reactive T cells are not sensitive to Con A and thus these cells do not produce proliferative responses to IL 2. The molecular basis for this dysfunction is poorly understood. Push