Innate immune effector pathways

Innate immune effector pathways are the primary defense mechanisms used by the host to detect and respond to pathogens and cellular damage. These pathways are triggered by pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and the cGAS-STING system [1][2]. Activation leads to the production of pro-inflammatory cytokines, chemokines, and type I interferons, which coordinate the recruitment and activation of other immune cells [3]. In oncology, drugs like TLR agonists and STING agonists are used to stimulate these pathways within the tumor microenvironment to promote anti-tumor immunity [4]. In contrast, overactivation of these pathways is linked to chronic inflammatory diseases and autoimmunity, where inhibitors are employed to reduce tissue damage [5]. Key effector mechanisms also include the complement system and the formation of inflammasomes, which can trigger inflammatory cell death known as pyroptosis [6]. Because this term encompasses a broad set of biological processes rather than a single protein, it serves as a functional category for various therapeutic targets. [1] Janeway CA Jr, Medzhitov R. "Innate immune recognition." Annu Rev Immunol. 2002. [2] Takeuchi O, Akira S. "Pattern recognition receptors and inflammation." Cell. 2010. [3] Paludan SR, et al. "Innate immune mechanisms of nucleic acid sensing." Nat Rev Immunol. 2019. [4] Corrales L, et al. "The host STING pathway at the intersection of cancer and immunity." J Clin Invest. 2016. [5] Dinarello CA. "Interleukin-1 in the pathogenesis and treatment of inflammatory diseases." Blood. 2011. [6] Broz P, Dixit VM. "Inflammasomes: mechanism of assembly, regulation and signalling." Nat Rev Immunol. 2016.

Other names

Innate immunityInnate immune systemPattern recognition receptor pathwaysInnate immune signaling

Agonism or antagonism of pattern recognition receptors (PRRs) and downstream signaling components to modulate the production of cytokines and interferons.