“Toll-free” pathways for production of type I interferons

AIMS Allergy and Immunology

Ling Wang¹ 

[1] 1 Department of Internal Medicine, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA2 Center of Excellence for Inflammation, Infectious Diseases and Immunity, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA

关键词: PRR;    cGAS;    IFN-I;    innate immunity;   

DOI  :  10.3934/Allergy.2017.3.143

学科分类：医学（综合）

来源: American Institute of Mathematical Sciences

【 摘 要 】

Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) are recognized by different cellular pathogen recognition receptors (PRRs), which are expressed on cell membrane or in the cytoplasm of cells of the innate immune system. Nucleic acids derived from pathogens or from certain cellular conditions represent a large category of PAMPs/DAMPs that trigger production of type I interferons (IFN-I) in addition to pro-inflammatory cytokines, by specifically binding to intracellular Toll-like receptors or cytosolic receptors. These cytosolic receptors, which are not related to TLRs and we call them “Toll-free” receptors, include the RNA-sensing RIG-I like receptors (RLRs), the DNA-sensing HIN200 family, and cGAS, amongst others. Viruses have evolved myriad strategies to evoke both host cellular and viral factors to evade IFN-I-mediated innate immune responses, to facilitate their infection, replication, and establishment of latency. This review outlines these “Toll-free” innate immune pathways and recent updates on their regulation, with focus on cellular and viral factors with enzyme activities.

【 授权许可】

CC BY