| Regulation mechanism of IL-21/IL-21R signaling on T helper cell responses during affection forming in intestinal lamina propria by intestinal inflammation was investigated. In this study, IL-21R gene was used to knock off mice (IL-21RKO), and establish TNBS induced animal model of inflammatory enteric disease. Determined and tested body weight and survival rate of mice; HE staining to observe mice intestinal tissue structure and the conditions of inflammatory responses; isolated and separated intestinal lamina propria lymphocyte (LPL), and counted the Th1, Th2, Th17, and Treg cell proportion and absolute number applied with flow cytometer; ELISA to determine and test the secretion of cell factors (IFN-γ, IL-4, IL-17A, IL-10) in LPL culture supernatant. The results showed that as compared with WT mice, the body weight of IL-21R KO lose weight more quickly, and the survival rate reduced; HE staining showed that epithelium of mice intestinal duct got serious damage, recessus disappeared at large area, many inflammatory cells infiltrated, and invaded in muscularis mucosae; the Th1 cell response of IL-21R KO lamina propriae significantly enhanced, yet responses of Th2, Th17, and Treg contrarily inhibited. Therefore, IL-21/IL-21R signaling plays important protective role in the formation of TNBS induced enteritis affection in mice through regulating the Th cell response in their lamina propriae. |
