Studies on Experimental Autoimmune Gastritis.

出生后第3天切除胸腺，在2月龄时，51-73%的BALB/c小鼠和3 - 8%的DBA/2小鼠中诱导了自身免疫球蛋白（AIG）。组织学和血清学检查检测AIG。为了从遗传学上研究控制AIG发病的机制，使用了从这两个品系之间的F2建立的11个重组近交系。在检测的26个标记中，发现BALB/c第1号染色体上的Mls-1位点和第2号染色体上的Hc位点与AIG的高易感性相关。值得注意的是，与正常的BALB/c小鼠相比，在AIG小鼠的外周淋巴结中，已知对Mls-1 α抗原有应答的V β 6阳性B细胞增加。提示Mls-1 α抗原与AIG发病有密切关系。这一观点进一步得到以下发现的支持：大多数从AIG小鼠建立的T细胞克隆表达V β 6和CD 4，并且当转移到BALB/c nu/nu小鼠中时，两个体外特异性应答壁细胞的克隆引起对鼠胃提取物的DTH反应，但不引起对肝提取物的DTH反应。Mls-1^a抗原和壁细胞自身抗原的分子分析正在进行中，这些抗原是用单克隆自身抗体作为质子泵测定的。

Thymectomy on day 3 after birth induced Auto-Immune Gastritis (AIG) at the age of 2 months in 51-73% of BALB/c, and in 3& of DBA/2 mice. AIG was detected by histological and serological examination. To investigate genetically the mechanism controlling the incidence of AIG, 11 recombinant inbred strains established from F2 between these two strains were used. Among 26 markers tested, the Mls-1 locus on BALB/c chromosome 1 and the Hc locus on BALB/c chromosome 2 were found to be associated with high susceptibility to AIG. It was noted that Vbeta6-positive B cells which are known to be responders to Mls-1^a antigens increased in the peripheral lymph nodes of AIG mice compared to normal BALB/c mice. This suggests an intimate relationship between Mls-1^a antigens and pathogenesis of AIG. This notion was further supported by findings that most of T cell clones established from AIGmice expressed Vbeta6 together with CD4 and that two clones specifically responding to parietal cells in vitro caused DTH reaction to murine gastric extract, but not to liver extract when transferred into BALB/c nu/nu mice. Molecular anlysis of Mls-1^a antigens and parietal cell autoantigens which were determined by using monoclonal autoantibodies as proton pump is in progress.