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Figure adapted from Patra MC, Choi S. Molecules. 2016;21(11):1-16; Chaudhary D et al. J Med Chem. 2015;58(1):96-110;
O'Neill LAJ. Immunol Rev. 2008;226:10-18.

  • The Toll-like and interleukin-1 receptors are primary mediators of innate immunity4,5
  • Activation of these receptors by endogenous ligands can result in increased expression of proinflammatory cytokines such as tumor necrosis factor α and IL-8, thus triggering the inflammatory and immune response9-12
  • In mice with genetically deleted IRAK4, the TLR/IL-1 signaling is severely impaired, suggesting that IRAK4 plays a key role in innate immunity. Humans with mutations in the IRAK4 gene have impaired innate and acquired immunity and may be susceptible to clinically important recurrent infections1,2,13,14
  • Toll receptor activity is increased in rheumatoid arthritis; increased TLR signaling and IRAK4 activation may explain the pathogenesis and progression of this disease4,5,9