Kweon M N, Yamamoto M, Kajiki M, Takahashi I, Kiyono H
Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
J Clin Invest. 2000 Jul;106(2):199-206. doi: 10.1172/JCI8490.
Systemically primed BALB/c mice developed severe diarrhea after repeated oral administration of ovalbumin (OVA). Histological analysis demonstrated that dramatic infiltration of eosinophils and mast cells occurred in the large intestine but not in the small intestine of mice with diarrhea. Interestingly, CD4(+) alphabeta T cells of the large intestine secreted IL-4 and IL-13 at high levels. Identically treated STAT6 gene-disrupted mice failed to develop OVA-induced diarrhea. Further, treatment of BALB/c mice with monoclonal anti-IL-4 antibody prevented the development of allergic diarrhea. An adoptive transfer study showed that systemically primed splenic CD4(+) T cells were preferentially recruited into the large intestine upon exposure to oral OVA. These results strongly suggest that systemically derived CD4(+) alphabeta T cells of the large intestine play a critical role in the onset of Th2-mediated intestinal allergic disorders via STAT6 signal transduction.
经全身致敏的BALB/c小鼠在反复口服卵清蛋白（OVA）后出现严重腹泻。组织学分析表明，腹泻小鼠的大肠中出现了嗜酸性粒细胞和肥大细胞的大量浸润，而小肠中未出现。有趣的是，大肠中的CD4(+)αβ T细胞高水平分泌IL-4和IL-13。经相同处理的STAT6基因敲除小鼠未能出现OVA诱导的腹泻。此外，用单克隆抗IL-4抗体处理BALB/c小鼠可预防过敏性腹泻的发生。一项过继转移研究表明，经全身致敏的脾CD4(+) T细胞在接触口服OVA后优先被募集到大肠中。这些结果强烈表明，大肠中系统性来源的CD4(+)αβ T细胞通过STAT6信号转导在Th2介导的肠道过敏性疾病的发病中起关键作用。
