TLR2 signaling is essential in regulating dendritic cells function during porcine epidemic diarrhea virus infection.

The innate immune system serves as the first line of defense for the host against microbial invasion. Toll-like receptors (TLRs), are pathogen pattern recognition receptors can initiate signal cascades to mediate innate immune responses; however, the mechanism of TLR2 in viral infections remains unclear. This study aimed to clarify the impact of TLR2 deficiency on the pathogenesis of Porcine Epidemic Diarrhea Virus (PEDV) infection and host immune defense. Through transcriptome analysis, the abnormal molecular expression profiles induced by TLR2 deficiency in PEDV-infected bone marrow-derived dendritic cells (BMDCs) was characterised, including aberrant activation of the non-canonical nuclear factor-kappa B (NF-κB) signaling pathway, dysregulated expression of MHC Class Ⅰ/Ⅱ genes, and disordered apoptotic signaling. To verify the effects of these molecular characteristics on cellular functions, further detection using flow cytometry revealed the following: in terms of maturation and activation, TLR2 deficiency significantly reduced the surface levels of CD40+, CD86+, and CD83+ in PEDV-infected BMDCs (p < 0.05); regarding antigen-presenting function, IFN-γ+ expression was significantly downregulated in CD4+/CD8+ T cells co-cultured with TLR2-deficient BMDCs (p < 0.05). The level of late apoptosis in TLR2-deficient BMDCs was significantly increased (p < 0.05). In summary, TLR2 deficiency can lead to defects in maturation and activation, impaired antigen-presenting function, and enhanced apoptosis in PEDV-infected BMDCs, a process that may be associated with the aberrant activation of the non-canonical NF-κB pathway mediated by TLR2 deficiency. This study provides new insights at the molecular and cellular levels for elucidating the role of TLR2 in PEDV infection and host immune defense.