The core of this was how the single immunoglobulin interleukin-1 receptor-related protein influenced the signaling pathways of NK cells, Th1 cells, and TLRs to exert its immunosuppressive effect...
Wu Ting began to sketch schematic diagrams detailing the precise mechanisms of these cells and signaling pathways in chronic hepatitis B...
After working through his deductions, Wu Ting distilled it all into a final summary:
The complete immunomodulatory mechanism:
SIGIRR-based therapy would activate TLR4 through negative feedback. This would elevate levels of pro-inflammatory cytokines, such as NKG2A on the surface of NK cells, as well as IL-6 and TNF-α. Consequently, anti-inflammatory cytokines like IFN-γ, IL-10, and IL-18 would decrease, ultimately triggering immunosuppression...
