IgG4+ plasma cell infiltration is correlated with the development of inflammatory bowel disease and can be regulated by TLR-4.

Immunoglobulin 4 (IgG4) is commonly considered a hallmark of autoimmune pancreatitis (AIP). Inflammatory bowel disease (IBD) is believed to play a substantial role in the setting of AIP. Toll-like receptor 4 (TLR4) plays an important role in inflammation. The relationship between IgG4 and TLR4 in the process of IBD is incompletely explored. Our study aimed to assess the expression of IgG4 and TLR4 in IBD patients and to find the role of IgG4 and TLR4 in the IBD process. A cohort of 68 IBD patients was enrolled in our study, and 20 healthy persons served as a control group. Intestinal IgG4 positive (IgG4+) plasma cell infiltration was measured by immunohistochemistry. Serum IgG4 and TLR4 levels were measured by ELISA. Fifteen additional features from the patients' general medical information and lab data were also collected to assess the risk factors of IBD activity by logistical analysis. BALB/c mice were used to build a rat IBD model with dextran sulfate sodium (DSS). The TLR4 inhibitor TAK242 was used to regulate the expression of TLR4. The expression of IgG4 and TLR4 in serum was detected by ELISA. The expression of IgG4 and TLR4 in the intestines were assayed with western blot. Our results revealed that the infiltration of IgG4+ plasma cells was higher in IBD patients (14/68 vs 0/20, P<0.05). The incidence of IgG4+ plasma cells in the IBD group (48.5%) was higher than in the control group (33/68 vs 0/20, P<0.05). Serum IgG4 and TLR4 levels in the IBD group were significantly higher compared with the control group (P<0.05). Based on our logistical analysis, three variables: IgG4+ plasma cell infiltration, CRP, and HB were identified as independent risk factors with odds ratios of 10.917, 1.031, and 0.923, respectively (