PATHOGENESIS OF AUTOIMMUNITY IN MICE WITH SLE-LIKE ILLNESS

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细胞激活，随后优先 (可能是抗原依赖和T细胞依赖)自身抗体 制作。 所有的自身免疫小鼠品系，但不是大多数正常品系 小鼠表达全长(8.4 kb)MCF逆转录病毒转录本 胸腺和脾。NZB小鼠从出生起就有这样的转录 这表明它们不是疾病造成的。多克隆免疫 激活剂可以诱导至少一个8.4kb的MCF逆转录病毒 在小鼠中发现了转录本；然而，还发现了额外的转录本(S) 在未受刺激的自身免疫小鼠中。 GLD基因已被定位到小鼠染色体远端的一个区域 与人类1号染色体同源并具有紧密连锁的1号染色体 三点到三点。

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.