ara-lipoarabinomannan, NF-kB, MD-2, IL-8, TLR2, pneumolysin, Fibronectin, TLR7, c-Jun, CD14, TOLLIP, TRAF6, IL-6, IP10, p38beta (MAPK11), NIK(MAP3K14), MyD88, CCL20, I-TAC, LBP, LAM, single-stranded RNA, TLR9, TLR6, IKK-beta, Loxoribine, IKK (cat), IL-11, Eotaxin, LPS, IRAK1/2, Lipoteichoic acid, Lipoteichoic acid, Imiquimod, TLR5, Resiquimod, lipoprotein, IRAK4, TAB2, PSAP, IRAK1, TLR8, IRAKM, MEK3(MAP2K3), TIRAP (Mal), IL-4, CD14, TAB1, TLR4, TLR1, Flagellin, IFN-beta, I-kB, TAK1(MAP3K7), Zymosan, Bacterial DNA, Paclitaxel cytosol
TLR signaling pathways
Both gram-positive and gram-negative bacteria and their cell wall components activate innate immune system of the host and induce secretion of proinflammatory molecules, mainly chemokines and cytokines . Toll-like receptors (TLRs) initiate signaling cascades through recognition of a variety of microbial components, thus serving as an important link between innate and adaptive immune responses. Each TLR recognizes distinct ligands . TLR2 agonists include peptidoglycan, lipoproteins, and lipopeptides from Gram-positive bacteria, mycobacterial lipoarabinomannan, mycoplasma lipopeptides , but only when present as a heterodimer in combination with either TLR1 or TLR6 . TLR3 and TLR5 mediate cell activation by double-stranded viral RNA and bacterial flagellin, respectively . TLR9 responds to unmethylated CpG motif in bacterial DNA , . TLR4 is essential in the respective recognition of lipopolysaccharide ( LPS ) , lipoteichoic acid  and some other substrates , , . A number of microbial substrates are known for TLR7 and TLR8 , , .
The main TLR-mediated immune response pathway, which is common for all TLRs, is Myeloid differentiation primary response gene 88 ( MyD88 )-dependent activation of Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor ( NF-kB ) and c-Jun, transcription regulators of number of chemokines and cytokines responsible for cellular immune response. The main steps of NF-kB activation involve MyD88/ Interleukin-1 receptor-associated kinases ( IRAK )/ TNF receptor-associated factor 6 ( TRAF6 )/ Mitogen-activated protein kinase kinase kinase 14 ( NIK )/ Inhibitor of kappa light polypeptide gene enhancer in B-cells ( IKK )/ NF-kB signal transduction . C-Jun activation proceeds throw MyD88/ IRAK/ TRAF6/ Mitogen-activated protein kinase kinase kinase 7 interacting protein 1 ( TAB )/ Mitogen-activated protein kinase kinase kinase 7 ( TAK ) cascade , . Besides MyD88, some TLR s use alternative adaptor proteins to induce NF-kB and c-Jun activation, such as Toll-interleukin 1 receptor domain containing adaptor protein ( TIRAP ) , . Certain types of TLRs (for example, TLR3 and TLR4 ) demonstrate also other response pathways, which are specific for them.