TLR2/NF-κB signaling could oversee the function of CD56bright NK cells in patients afflicted with severe fever and thrombocytopenia syndrome (SFTS).

Severe fever with thrombocytopenia syndrome (SFTS), an emerging infectious disease caused by a novel bunyavirus, presents a significant threat due to its high mortality rate. Immune suppression is recognized as a crucial factor in the progression of this disease. NK cells, as effector cells in the innate immune system, play important immune functions. Toll-like receptors (TLRs), specifically pattern-recognition receptors, initiate the activation of intracellular signaling factors upon activation. However, there is a paucity of data regarding immune responses in SFTS. In this study, we aimed to investigate the changes in TLR2 and NF-κB within NK cells and examine how the TLR2/NF-κB signaling pathway affects NK cells during SFTS. Our findings revealed that in SFTS patients, there was an increase in the expression of TLR2 and NF-κB in both CD56dimCD16+ and CD56brightCD16- NK cell subsets. Additionally, the function of CD56bright NK cells was enhanced in SFTS patients after stimulation with Pam3CSK4. This suggests that TLR2 signaling plays a crucial role in activating and enhancing the function of CD56bright NK cells following SFTS virus infection. This research will facilitate a deeper understanding of the pathogenesis of SFTSV and could provide an immunological foundation for developing new therapeutic strategies.