IRAK-4: A key kinase involved in toll-like receptor signaling and resistance to bacterial infection

摘要: Extreme complexity and a potential for cross-talk within the TLR signaling pathways suggest that mutations in almost any receptors or intracellular components would result severe innate immune deficiency. However, to date, relatively few have been described underlie deficient TLR4 increased susceptibility infectious disease. These include TLR4, IRAK-4 enzyme, NEMO (IKKγ) IκBα of IKK complex. Due central role mediating TLR-mediated signal transduction, severely affect antibacterial defense mechanisms. This defect is associated with kinase domain seem inhibit formation functional complexes receptor IL-1R/TLR4 pathway. property truncated molecules also raises possibility therapeutic intervention hyperinflammatory states by using mimetics signaling. Future studies will likely reveal feasibility such an approach, delineate how deficiency affects other mechanisms, including development adaptive immunity.