Penney I, Kilshaw P J, MacDonald T T
Department of Paediatric Gastroenterology, St. Bartholomew's Hospital, London, UK.
Immunology. 1996 Sep;89(1):54-8. doi: 10.1046/j.1365-2567.1996.d01-721.x.
Cholera toxin (CT) or its subunits were given orally to mice and division of intestinal intraepithelial lymphocytes (IEL) in vivo measured by double immunofluorescence using 5-bromo-2'-deoxyuridine (BRdU) and membrane alpha beta T-cell receptors (TCR) or gamma delta TCR staining in frozen sections. Cholera toxin (10 micrograms) produced a two- to eightfold-increase in the uptake of BRdU in alpha beta TCR+ IEL in the duodenum and a two-to fivefold increase in gamma delta TCR IEL in the ileum. Increased uptake of BRdU was also seen after a dose of 100 micrograms of CT but this dose was also associated with the loss of alpha beta TCR+ IEL and gamma delta TCR+ IEL in the duodenum. CT-A and CT-B subunit produced increased BRdU incorporation by alpha beta TCR in the duodenum and by gamma delta TCR IEL in the ileum. Cholera toxin therefore appears to be mitogenic for IEL probably due to an indirect mechanism.
将霍乱毒素(CT)或其亚基经口给予小鼠,并通过在冰冻切片中使用5-溴-2'-脱氧尿苷(BRdU)和膜αβT细胞受体(TCR)或γδTCR染色,采用双重免疫荧光法在体内测量肠道上皮内淋巴细胞(IEL)的分裂情况。霍乱毒素(10微克)使十二指肠中αβTCR + IEL的BRdU摄取增加了2至8倍,回肠中γδTCR IEL的BRdU摄取增加了2至5倍。给予100微克CT剂量后也观察到BRdU摄取增加,但该剂量也与十二指肠中αβTCR + IEL和γδTCR + IEL的减少有关。CT-A和CT-B亚基使十二指肠中的αβTCR以及回肠中的γδTCR IEL的BRdU掺入增加。因此,霍乱毒素似乎对IEL具有促有丝分裂作用,可能是由于一种间接机制。