Differential response of porcine immature monocyte-derived dendritic cells to virulent and inactivated transmissible gastroenteritis virus

- Virulent TGEV down-regulates cell surface markers of immature Mo-DCs.
- Virulent TGEV limits the immature Mo-DCs to secrete IL-12, IFN-γ and IL-10.
- Virulent TGEV impairs the ability of immature Mo-DCs to stimulate T cell proliferation.
- Virulent TGEV inhibits the activation of nuclear factor kappa B (NF-κB) in immature Mo-DCs.
- UV-inactivated TGEV (UV-SHXB) has the opposite effects in immature Mo-DCs.

Exposure of piglets less than 2 weeks of age to virulent transmissible gastroenteritis virus (TGEV) gives rise to mortality as high as 100%, and adult pigs recovering from its infection often become TGEV carriers. These facts suggest an evasion of the immune system by virulent TGEV. In this study, we showed that a virulent TGEV SHXB strain could infect porcine immature monocyte-derived dendritic cells (Mo-DCs), and down-regulate cell surface markers (SLA-II-DR, CD1a and CD80/86). Moreover, SHXB-infected immature Mo-DCs showed low expression of IL-12 and IFN-γ, and also lost the ability to stimulate T cell proliferation. Finally, SHXB inhibited the activation of nuclear factor kappa B (NF-κB) in these cells. Instead, UV-inactivated SHXB (UV-SHXB) had the opposite effects in immature Mo-DCs. In conclusion, the virulent SHXB could severely impair immature Mo-DCs, which might be involved in the pathogenesis of virulent TGEV in vivo.