Role of Cytokines and Toll-Like Receptors in the Immunopathogenesis of Guillain-Barré Syndrome

Figure 2

TLR4 signaling during the host-pathogen interaction: pattern recognition receptors (PRRs) recognize evolutionary conserved repetitive structures such as lipid A in LPS present in Campylobacter jejuni and various other microorganisms. Stimulation of TLR4 by LPS facilitates the activation of two pathways: the MyD88- (myeloid differentiation primary-response protein 88-) dependent and MyD88-independent pathways (not shown). Downstream of TLR4 signaling involves different types of adaptor molecules which depend on the type of LPS and result in early phase of NF-B activation, which leads to the production of inflammatory cytokines. LPS, lipopolysaccharide; LBP, lipopolysaccharide binding protein; TLR4, toll-like receptor 4; MAL, MyD88 adaptor-like; TRIF, TIR domain-containing adaptor-inducing IFN-β; TRAF, TNF receptor-associated factors; TIRAP, toll-interleukin 1 receptor (TIR) domain-containing adaptor protein; IRAK, IL-1 receptor-associated kinase; TAK, TGFβ-activated kinase; IKKB, IB kinases; NF-B, nuclear factor kappa-light-chain-enhancer of activated B cells.