Studies on Experimental Autoimmune Gastritis.

51-73%的BALB/c小鼠和3%的DBA/2小鼠在出生后第3天切除胸腺，在2月龄时诱发自身免疫性胃炎（AIG）。通过组织学和血清学检查检测AIG。为了从遗传学角度探讨控制AIG发生的机制，利用这两株菌株之间的F2建立了11株重组近交系。在检测的26个标记中，发现BALB/c 1号染色体上的Mls-1位点和BALB/c 2号染色体上的Hc位点与AIG高易感性相关。值得注意的是，与正常的BALB/c小鼠相比，AIG小鼠周围淋巴结中的vbeta6阳性B细胞（已知对Mls-1^a抗原有反应）增加。提示Mls-1^a抗原与AIG的发病机制密切相关。研究结果进一步支持了这一观点，大多数由aig小鼠建立的T细胞克隆都表达Vbeta6和CD4，并且体外特异性应答壁细胞的两个克隆在转移到BALB/c nu/nu小鼠时对小鼠胃提取物产生DTH反应，而对肝脏提取物没有反应。用单克隆自身抗体作为质子泵测定Mls-1^a抗原和壁细胞自身抗原的分子分析正在进行中。

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.