Transmissible Gastroenteritis Virus Infection Up-Regulates FcRn Expression via Nucleocapsid Protein and Secretion of TGF-ß in Porcine Intestinal Epithelial Cells

Qian, Shaoju; Gao, Zitong; Cao, Rui; Yang, Kang; Cui, Yijie; Li, Shaowen; Meng, Xianrong; He, Qigai; Li, Zili

Transgenic mice that overexpress hFcRn can improve the antigen presentation ability of dendritic cells and enhance the humoral immune response of the body (Végh et al., 2012) . FcRn not only transports IgG, but also transports antigen-antibody complexes, which are taken up by antigenpresenting cells (APCs) (Rath et al., 2013) . When the pathogen stimulates the mucosal epithelium, the expression of FcRn may be regulated. Simian/human immunodeficiency virus (SHIV) infection decreases FcRn and pIgR expression, which may also be the mechanism responsible for its pathogenesis in rhesus monkeys (Wang and Yang, 2016) . On the other hand, TGEV up-regulates FcRn expression, which is potentially what provides the mucosal protection. To observe and measure IgG transcytosis in vitro, we applied the transwell system to mimic the porcine intestinal microenvironment, using IPEC-J2 cells to construct the transwell model, our previous research showed that FcRn not only transports specific antibodies across the mucosal epithelium in vitro, but also reduces the yield of TGEV (Guo et al., 2016a) . We speculated that the up-regulation of FcRn by N protein may mediates more TGEV-specific antibody transcytosis across the mucosal epithelium, thereby enhancing the host's anti-infective ability. On the other hand, N protein-enhanced FcRn mediates more IgG immune complex transcytosis, followed by antigen uptake by specialized APCs to activate adaptive immune responses. Overall, we elucidated the immune mechanism of TGEV induced FcRn expression and provided a scientific and theoretical basis for the prevention and control of TGEV infection.