Fig. 3.

Immune signaling pathways involved in MTB infection in vivo. MTB infection triggers immune responses by activating various Toll-like receptors (TLRs) through binding to a range of lipoproteins and lipopolysaccharides. MTB secretes specific antigens (Rv0577, Rv2660c, Rv3875, Rv3628, Rv2873, and Rv1808) that are recognized by TLR2, leading to dendritic cell maturation and the induction of Th1/Th17 response in tuberculosis immunity and inflammatory reactions. Similar to TLR2, TLR4 recognizes MTB antigens (Rv3478, Rv3417c, Rv0440, Rv0652, Rv0475, Rv1009, and 38 kD glycoprotein) in conjunction with dectin-1, resulting in apoptosis of MTB-infected macrophages and the production of IL-17A. Additionally, TLR9 recognizes MTB’s CpG DNA, promoting IFN-α production and regulating the Th1/Th2 balance. TBK1 TANK-binding kinase 1, TIRAP Toll/interleukin 1 receptor domain-containing adaptor protein, TRAF3 tumor necrosis factor receptor factor 3, IRF7 interferon regulatory factor 7, type I IFN type I interferon, TRIF Toll/interleukin 1 receptor-domain-containing adapter-inducing interferon-β, TAK1 transforming growth factor β activated kinase 1, IKKs inhibitor of nuclear factor κB kinases, NF-κB nuclear factor κB, IFN-γ interferon-γ, TNF-α tumor necrosis factor-α, IL interleukins