Immunization with gastric H+/K+‐ATPase induces a reversible autoimmune gastritis
Immunization with gastric H+/K+‐ATPase induces a reversible autoimmune gastritis
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胃 H+/K+-ATP 酶免疫诱导可逆性自身免疫性胃炎
DOI：
10.1046/j.1365-2567.1997.00302.x
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发表时间：
1997
期刊：
影响因子：
6.4
通讯作者：
B. Toh
中科院分区：
文献类型：
--
作者：
K. J. Scarff;J. Pettitt;I. V. Driel;Paul A. Gleeson;B. Toh
胃H+/K+-ATP酶被认为是人类恶性贫血和小鼠胸腺切除术诱导的自身免疫性胃炎的主要自身抗原。在这里，我们已经表明，可以通过用完全弗氏佐剂中的小鼠胃H+/K+-ATP酶直接免疫未切除胸腺的BALB/c小鼠来产生自身免疫性胃炎。胃炎的特征为胃粘膜下层和粘膜浸润巨噬细胞、CD 4+和CD 8 + T细胞和B细胞，以及循环的H+/K+-ATP酶自身抗体。 胃粘膜内的单核细胞浸润伴随着壁细胞和酶原细胞的丢失以及小的未成熟上皮细胞的积聚。来自胃炎小鼠的脾细胞将胃炎过继性转移给未感染的受体。停止免疫导致自身抗体滴度下降以及壁细胞和产酶细胞的再生。结果直接证实胃H+/K+-ATP酶是自身免疫性胃炎发生中的致病性自身抗原。免疫停止后病变的恢复表明，自我平衡机制可以逆转破坏性的自身免疫过程。
The gastric H+/K+‐ATPase has been implicated as a major autoantigen in pernicious anaemia in humans and in thymectomy‐induced autoimmune gastritis in mice. Here we have shown that autoimmune gastritis can be generated by direct immunization of non‐thymectomized BALB/c mice with mouse gastric H+/K+‐ATPase in complete Freund’s adjuvant. The gastritis was characterized by infiltration of the gastric submucosa and mucosa with macrophages, CD4+ and CD8+ T cells, and B cells and by circulating autoantibodies to the H+/K+‐ATPase. The mononuclear infiltrate within the gastric mucosa was accompanied by loss of parietal and zymogenic cells and accumulation of small immature epithelial cells. Splenocytes from gastritic mice adoptively transferred gastritis to naive recipients. Cessation of immunization resulted in decrease in autoantibody titre and regeneration of parietal and zymogenic cells. The results directly confirm that the gastric H+/K+‐ATPase is the causative autoantigen in the genesis of autoimmune gastritis. Recovery of the lesion following cessation of immunization suggests that homeostatic mechanisms can reverse a destructive autoimmune process.