Toll-like Receptors and NOD-like Receptors in Innate Immune Defense during Pathogenic Infection.
10.4167/jbv.2014.44.3.215
- Author:
Hyo Sun JIN
1
;
Jeong Kyu PARK
;
Eun Kyeong JO
Author Information
1. Department of Microbiology, Chungnam National University School of Medicine, Daejeon, Korea. hayoungj@cnu.ac.kr
- Publication Type:Review
- Keywords:
Toll-like receptors;
Nod-like receptors;
Inflammasome;
Host defense;
Infection;
Innate immunity
- MeSH:
Immune System;
Immunity, Innate;
Inflammation;
Insects;
Interleukin-1beta;
Mammals;
Toll-Like Receptors*
- From:Journal of Bacteriology and Virology
2014;44(3):215-225
- CountryRepublic of Korea
- Language:English
-
Abstract:
In response to invading pathogens, the body immune system develops an immediate defense mechanism, i.e., innate immune response, which is detected in almost all living organisms including mammals, plants, insects, etc. Recent studies have identified numerous innate immune receptors that are able to recognize pathogen-associated molecular patterns and transduce the essential intracellular signaling cascades to mount early and successful host defenses against infectious challenge. Among innate immune receptors, we will focus on two important receptors, toll-like receptors (TLRs) and nucleotide binding oligomerization domain (Nod)-like receptors, and their major intracellular signaling pathways that culminate to activate innate immune effectors and inflammatory mediators during pathogen infection. In this review, we address the recent advances of understanding intracellular signaling mechanisms by which TLRs and NLRs activate host immune defense and inflammation. The role and regulatory mechanisms by which a subet of NLRs-associated inflammasome activation induce interleukin-1beta secretion and their relevance with host defense will be also discussed. Both TLR- and NLR-mediated intracellular signaling networks serve crucial roles in mounting resistance to bacterial and viral infection through synthesis of immune mediators and antimicrobial chemicals during infection.
