The Innate Immune Responses in Pathogenesis of Chronic Rhinosinusitis.
- Author:
Ji Hun MO
1
Author Information
1. Department of Otorhinolaryngology, Dankook University College of Medicine, Cheonan, Korea. jihunmo@gmail.com
- Publication Type:Review
- Keywords:
Chronic Rhinosinusitis;
Innate Immunity;
Toll-Like Receptors;
Barrier Function;
Innate Lymphoid Cells
- MeSH:
Adaptive Immunity;
Fungi;
Immune System;
Immunity, Innate*;
Inflammation;
Receptors, Pattern Recognition;
Superantigens;
Toll-Like Receptors
- From:Journal of Rhinology
2014;21(1):22-27
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Chronic rhinosinusitis (CRS) is a multifactorial and heterogeneous disease, and variousfactors, such as inflammation, infection, fungus, and superantigens, have been proposed to play crucial roles in its pathogenesis. Recently, the dominant mechanismof CRS pathogenesis has shiftedfrom microbial infection and environmental factors to host susceptibility. Host susceptibility relies not only on adaptive immunity, but also on innate immunity, and there has recently been much research into innate immunity. Innate immunity is an evolutionally conserved immune system that recognizes microbial signature molecules via pattern recognition receptors and is a primary defense system that elicits inflammatory and bactericidal responses. Dysfunction of the host response to pathogens is suggested to be involved in pathogenesis of CRS and an irrelevant response of the host's innate immunity could cause a failure toeradicate the pathogens, thereby contributing to CRS pathogeneses. Among these innate immune systems, toll-like receptors and epithelial barrier functions have been studied extensively, and new players, such as innate lymphoid cells,have beensurfacing. Betterunderstanding of innate immunity couldhelp to investigateand treat this complex disease. In this review, toll-like receptors, epithelial barrier functions, and innate lymphoid cells,among many subjects related to innate immunity,will be discussed in terms of pathogenesis.
