PATHOGENESIS OF AUTOIMMUNITY IN MICE WITH SLE-LIKE ILLNESS

新西兰小鼠的自身免疫具有遗传和免疫性 然而，表达的严重性可以通过病毒修饰， 以及其他环境因素和性激素。 的 免疫因素是复杂的。 包括B细胞过多 活化和异常T细胞功能。 一个单一的基因，xid，防止疾病在同类NZB和（NZB x NZW（F1和BXSB小鼠），并显著延缓MRL- 1pr/lpr小鼠。 BXSB小鼠具有Y染色体连锁基因 它能加速自身免疫小鼠的自身免疫， 而不是在非自身免疫小鼠中引起。 对NZB、BXSB、MRL-lpr/lpr和正常小鼠的研究表明， 它们的B细胞库非常相似，这表明B 这些小鼠中的细胞活化由多克隆活化诱导。 不同的自身免疫性小鼠具有增加的 不同的细胞癌基因。 lpr/lpr和gld/gld小鼠具有 增加myb和T细胞受体（β基因）mRNA。 的xid 基因阻止了myc和ras表达的增加， NZB和BXSB小鼠，表明癌基因与 B细胞活化和自身抗体产生。 的研究 lpr/lpr小鼠的基因表达指出了一条新的途径 for T cell细胞maturation成熟.

Autoimmunity in New Zealand mice has a genetic and immune basis; however, severity of expression can be modified by viral and other environmental factors as well as sex hormones. The immune factors are complex. These include excessive B-cell activation and abnormal T cell function. A single gene, xid, prevents disease in congenic NZB and (NZB x NZW(F1 and BXSB mice, and markedly retards disease in MRL- 1pr/lpr mice. BXSB mice have a Y chromosome-linked gene which accelerate autoimmunity in autoimmune mice, but does not cause it in non-autoimmune mice. Studies of NZB, BXSB, MRL-lpr/lpr and normal mice show that the repertoires of their B cells are very similar suggesting that B cell activation in these mice is induced by polyclonal activation. Different autoimmune mice have increased expression of different cellular oncogenes. Lpr/lpr and gld/gld mice have increased myb and T cell receptor (Beta gene) mRNA. The xid gene prevents increased myc and ras expression characteristic of NZB and BXSB mice, suggesting that oncogene is associated with B cell activation and autoantibody production. The studies of gene expression in lpr/lpr mice have pointed to a new pathway for T cell maturation.