Kemp J D, Cowdery J S, Steinberg A D, Gershon R K
J Immunol. 1982 Jan;128(1):388-92.
A genetic experiment has been performed in mice to test the B cell "hyperactivity" hypothesis of autoantibody production. A backcross was designed such that some progeny carried both the sex-linked recessive gene xid, which markedly reduces the B cell hyperactivity and autoantibody production seen in NZB mice, and the autosomal recessive gene Ipr, which produces a severe lymphoproliferative/autoimmune disorder in the homozygous animal. The data indicate that although xid does not preclude any measured phenotypic expression of Ipr/Ipr disease, it may play a minor modulatory role. In addition, a background gene or genes in the CBA/N mouse, distinct from xid, modulates T cell proliferation in male backcross progeny. This experiment supports the view that autoimmune phenomena are fundamentally heterogeneous, and may involve complex cellular interactions.
已在小鼠中进行了一项基因实验，以检验自身抗体产生的B细胞“活性过高”假说。设计了一种回交方式，使得一些后代同时携带性连锁隐性基因xid（该基因可显著降低在NZB小鼠中观察到的B细胞活性过高和自身抗体产生）和常染色体隐性基因Ipr（该基因在纯合动物中会引发严重的淋巴细胞增生/自身免疫性疾病）。数据表明，尽管xid并不排除Ipr/Ipr疾病任何可测量的表型表达，但它可能发挥较小的调节作用。此外，CBA/N小鼠中与xid不同的一个或多个背景基因可调节雄性回交后代中的T细胞增殖。该实验支持了自身免疫现象本质上具有异质性且可能涉及复杂细胞相互作用的观点。
