Molecular biology of autoinflammatory diseases

被引：18

作者：

Masumoto, Junya ^{[1
]}

Zhou, Wei

Morikawa, Shinnosuke

Hosokawa, Sho

Taguchi, Haruka

Yamamoto, Toshihiro

Kurata, Mie

Kaneko, Naoe

机构：

[1] Ehime Univ, Grad Sch Med, Dept Pathol, Shitsukawa 454, Toon, Ehime 7910295, Japan

来源：

INFLAMMATION AND REGENERATION | 2021年 / 41卷 / 01期

关键词：

Interleukin-1; NF-kappa B; Type I interferon; Autoinflammatory diseases; NF-KAPPA-B; CONTAINING APAF1-LIKE PROTEIN; NLRP3; INFLAMMASOME; PERIODIC FEVER; RIG-I; REGULATES ACTIVATION; CASPASE-1; ACTIVATION; PYRIN INFLAMMASOME; CARD15; MUTATIONS; INNATE IMMUNITY;

D O I：

10.1186/s41232-021-00181-8

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The long battle between humans and various physical, chemical, and biological insults that cause cell injury (e.g., products of tissue damage, metabolites, and/or infections) have led to the evolution of various adaptive responses. These responses are triggered by recognition of damage-associated molecular patterns (DAMPs) and/or pathogen-associated molecular patterns (PAMPs), usually by cells of the innate immune system. DAMPs and PAMPs are recognized by pattern recognition receptors (PRRs) expressed by innate immune cells; this recognition triggers inflammation. Autoinflammatory diseases are strongly associated with dysregulation of PRR interactomes, which include inflammasomes, NF-kappa B-activating signalosomes, type I interferon-inducing signalosomes, and immuno-proteasome; disruptions of regulation of these interactomes leads to inflammasomopathies, relopathies, interferonopathies, and proteasome-associated autoinflammatory syndromes, respectively. In this review, we discuss the currently accepted molecular mechanisms underlying several autoinflammatory diseases.

引用

页数：26

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