IRAK-4--a shared NF-kappaB activator in innate and acquired immunity.
The human body is protected against external pathogens by two immune systems: innate and acquired immunities. Whereas innate immunity exhibits immediate responses to external pathogens by recognizing pathogen-associated molecular patterns (PAMPs), adaptive immunity uses T cells to recognize and defend against pathogens by developing effector cells, antibodies and memory cells. Although each system seems to possess distinct activation mechanisms, interleukin-1 receptor-associated kinase (IRAK)-4 is essential for NF-kappaB activation in Toll-like receptor (TLR) and T-cell receptor (TCR) signaling pathways. This implies possible crosstalk between innate and acquired immunities, and evolutionary development that resulted in the use of innate signaling molecules by the acquired immune system. Here, we discuss the impact of these evolutionarily conserved molecules on innate and acquired immunity, and their potential as drug targets for the simultaneous modulation of both immunities.
Suzuki
Nobutaka
N
Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan. nobu@rcai.riken.jp
Saito
Takashi
T
D000293:Adolescent; D000818:Animals; D001402:B-Lymphocytes / Q000378:metabolism; D017124:Conserved Sequence; D019143:Evolution, Molecular; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007113:Immunity, Innate; D053592:Interleukin-1 Receptor-Associated Kinases / Q000172:deficiency / Q000502:physiology*; D051379:Mice; D018448:Models, Immunological; D016328:NF-kappa B / Q000378:metabolism*; D020239:Receptor Cross-Talk; D011948:Receptors, Antigen, T-Cell / Q000378:metabolism / Q000502:physiology; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000473:pathology
D016328:NF-kappa B; D011948:Receptors, Antigen, T-Cell; D053592:Interleukin-1 Receptor-Associated Kinases