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

Transmissible gastroenteritis virus replication occurs in the small intestinal epithelial cells, while viral entry and release are restricted to the apical surface of polarized epithelial cells. Neonatal Fc receptor (FcRn) is a specific receptor for the immunoglobulin IgG, which is expressed in many cells, including epithelial cells, macrophages, and dendritic cells (Ye et al., 2008) . FcRn transports of IgG in the female reproductive tract plays an important role in combating infection (Li et al., 2011) . In addition to IgG, FcRn binds albumin, which regulates liver damage (Pyzik et al., 2017) . It has been found that FcRn can enhance HIV-I endocytosis in transmucosal epithelial cells (Gupta et al., 2013) . It has also been documented that the use of fusion proteins of the Fc fragment as immunogenic antigens can improve the impact of vaccines. Intranasally inoculated fusion protein, HSV-2 gD, HIV Gag fused with the Fc region of IgG, and targeted FcRn can all induce systemic and mucosal immunity to genital infections (Lu et al., 2011; Ye et al., 2011) . Most studies on FcRn have focused on the function of FcRn in humans and mice; so far, only a few relevant studies about pathogenic infection and FcRn expression regulation have been reported. In our previous study, TGEV induced FcRn expression via the NF-κB pathway in IPEC-J2 cells (Guo et al., 2016b) , but the regulatory mechanisms underlying this remain unclear; thus, we need to further explore the involvement of pattern recognition receptors (PRRs), inflammatory factors, and virus-coding proteins in the regulation of FcRn.