Mammals sense pathogen invasion through pattern-recognition receptors (PRRs). A group of transmembrane proteins, Toll-like receptors (TLRs) are mainly expressed on antigen-presenting cells, such as macrophages or dendritic cells, and play critical roles as PRRs (1). TLR signaling activates antigen-presenting cells that provoke innate immunity and establish adaptive immunity. TLRs can be activated not only by invading pathogens but also by certain danger or stress-associated endogenous molecules leading to the induction of sterile inflammation. Activation of TLRs is a first line defense of the immune system, leading not only to the activation and recruitment of neutrophils and macrophages to sites of infection, but also to the enhancement of antimicrobial activity (2). Each TLR has common effects, such as inflammatory cytokine induction or upregulation of costimulatory molecule expression. However, TLRs also have specific functions, exemplified by type I IFN-inducing ability. These immunoadjuvant effects are critical in antimicrobial immunity and also involved in manifestations of autoimmunity (1). Therefore, understanding the molecular mechanisms of TLRs should facilitate the development of therapeutic solutions for allergy and autoimmune diseases.