Kamal M, Wakelin D, Ouellette A J, Smith A, Podolsky D K, Mahida Y R
Division of Gastroenterology, University of Nottingham, UK.
Clin Exp Immunol. 2001 Oct;126(1):117-25. doi: 10.1046/j.1365-2249.2001.01589.x.
Secretions of Paneth, intermediate and goblet cells have been implicated in innate intestinal host defense. We have investigated the role of T cells in effecting alterations in small intestinal epithelial cell populations induced by infection with the nematode Trichinella spiralis. Small intestinal tissue sections from euthymic and athymic (nude) mice, and mice with combined deficiency in T-cell receptor beta and delta genes [TCR(beta/delta)-/-] infected orally with T. spiralis larvae, were examined by electron microscopy and after histochemical and lineage-specific immunohistochemical staining. Compared with uninfected controls, Paneth and intermediate cell numbers increased significantly in infected euthymic and nude mice but not infected TCR(beta/delta)-/- mice. Transfer of mesenteric lymph node cells before infection led to an increase in Paneth and intermediate cells in TCR(beta/delta)-/- mice. In infected euthymic mice, Paneth cells and intermediate cells expressed cryptdins (alpha-defensins) but not intestinal trefoil factor (ITF), and goblet cells expressed ITF but not cryptdins. In conclusion, a unique, likely thymic-independent population of mucosal T cells modulates innate small intestinal host defense in mice by increasing the number of Paneth and intermediate cells in response to T. spiralis infection.
潘氏细胞、中间细胞和杯状细胞的分泌物与肠道先天性宿主防御有关。我们研究了T细胞在由旋毛虫线虫感染引起的小肠上皮细胞群体变化中的作用。对经口感染旋毛虫幼虫的正常胸腺小鼠、无胸腺(裸)小鼠以及T细胞受体β和δ基因联合缺陷 [TCR(β/δ)-/-] 小鼠的小肠组织切片进行了电子显微镜检查,并进行了组织化学和谱系特异性免疫组织化学染色。与未感染的对照组相比,感染的正常胸腺小鼠和裸小鼠中潘氏细胞和中间细胞数量显著增加,但感染的TCR(β/δ)-/-小鼠中未增加。感染前转移肠系膜淋巴结细胞导致TCR(β/δ)-/-小鼠中潘氏细胞和中间细胞增加。在感染的正常胸腺小鼠中,潘氏细胞和中间细胞表达隐窝蛋白(α-防御素)但不表达肠三叶因子(ITF),杯状细胞表达ITF但不表达隐窝蛋白。总之,一种独特的、可能不依赖胸腺的黏膜T细胞群体通过在旋毛虫感染后增加潘氏细胞和中间细胞数量来调节小鼠小肠先天性宿主防御。