PATHOGENESIS OF AUTOIMMUNITY IN INBRED STRAINS OF MICE

近交系小鼠自身免疫的发病机制

• 批准号: 4688384
• 负责人: T M CHUSED
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/4688384
• 关键词: B lymphocyte; T lymphocyte; antibody formation; antibody specificity; autoantibody; autoimmune disorder; cell population study; flow cytometry; gene expression; genetic regulation; genetic strain; hybridomas; immunofluorescence technique; immunogenetics; immunoglobulin M; immunoglobulin genes; immunopathology chemotherapy; leukocyte activation /transformation; membrane reconstitution /synthesis; molecular pathology; secretory immune system; spleen

The genetic control and immunologic mechanisms of autoimmune disease is being investigated in the New Zealand strains of mice, their F1 hybrids, and recombinant-inbred lines derived from them. We have found 1) that enlargement of Lyt-2+ T cells is significantly associated with the titer of anti-erythrocyte autoantibody and degree of hemolytic anemia; 2) T cell suppression is defective in old NZB mice; 3) NZB, and particularly the (NZB x NZW) F1 hybrid, has a major resistance to induction of tolerance in the T cell subpopulation; 4) several abnormalities of proteins synthesized by lymphocytes from NZB mice can be demonstrated by two-dimensional gel electrophoresis. One, 16 kd in size, is observed only in enlarged NZB B cells, and may be associated with their pathologic spontaneous activation.

自身免疫性疾病的遗传控制和免疫机制是 在新西兰的小鼠菌株中进行了调查，他们的F1杂种， 和重组源性线从它们中得出。 我们发现1） Lyt-2+ T细胞的扩大与 抗肉芽肿自身抗体和溶血性贫血程度； 2）T细胞 抑制在旧的NZB小鼠中有缺陷； 3）NZB，尤其是（NZB） x nzw）f1杂种，具有诱导t的耐受性的主要抵抗力 细胞亚群； 4）由蛋白质合成的几种异常 NZB小鼠的淋巴细胞可以通过二维凝胶证明 电泳。 仅在扩大的NZB B中观察到一个，大小为16 kD 细胞，并且可能与它们的病理自发激活有关。