PATHOGENESIS OF AUTOIMMUNITY IN MICE WITH SLE-LIKE ILLNESS

患有系统性红斑狼疮样疾病的小鼠自身免疫的发病机制

• 批准号: 3819290
• 负责人: A D STEINBERG
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN 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/3819290
• 关键词: B lymphocyte; Retroviridae; antibody formation; autoantibody; autoimmune disorder; disease /disorder model; gene expression; genetic transcription; immunogenetics; laboratory mouse; leukocyte activation /transformation; linkage mapping; molecular pathology; systemic lupus erythematosus

Studies of antibody producing cells, including autoantibody producing cells, demonstrate that murine lupus is initiated by polyclonal B cell activation which is followed by preferential (probably antigen-dependent and T cell dependent) autoantibody production. All of the autoimmune mouse strains but not most normal strains of mice express full-length (8.4 kb) MCF retroviral transcripts in thymus, and spleen. NZB mice have such transcripts from birth suggesting that they do not result from disease. Polyclonal immune activators can induce at least one such 8.4 kb MCF retroviral transcript in NFS mice; however, additional transcript(s) are found in the unstimulated autoimmune mice. The gld gene has been mapped to a region of distal mouse chromosome 1 which is syntatic with human chromosome 1 and with close linkage to AT3.

抗体产生细胞的研究，包括自身抗体 产生细胞，证明小鼠狼疮是由 多克隆B细胞活化，随后优先 （可能是抗原依赖性和T细胞依赖性）自身抗体 生产 所有的自身免疫小鼠品系，但不是大多数正常的小鼠品系， 小鼠表达全长（8.4 kb）MCF逆转录病毒转录本， 胸腺和脾脏。 NZB小鼠从出生起就有这样的转录本 这表明它们不是由疾病引起的。 多克隆免疫 激活剂可以诱导至少一种这样的8.4kb MCF逆转录病毒 NFS小鼠中的转录本;然而，在小鼠中发现了额外的转录本。 在未受刺激的自身免疫小鼠中。 已将gld基因定位于小鼠染色体远端的一个区域 1号染色体与人类1号染色体共座， 到AT 3。