Premium
NLRP 3 “inflammasome” plays a central role in “inflammatory” demyelination of multiple sclerosis
Author(s) -
Yamamura Takashi
Publication year - 2013
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12082
Subject(s) - inflammasome , multiple sclerosis , innate immune system , caspase 1 , immunology , neuroscience , receptor , medicine , pyrin domain , disease , immune system , inflammation , biology , pathology
In the innate immune system, the NOD ‐like receptors recognize various pathogen‐associated and danger‐associated molecular patterns in immunocompetent cells. These diverse stimuli rapidly induce the formation of inflammasomes that serve as a molecular platform for efficient activation of caspase‐1, interleukin‐1β and interleukin‐18. Recent studies have shown that aberrant activation of NLRP 3 inflammasome plays a central role in inflammatory processes of gout, Crohn's disease and Alzheimer's disease. However, its role in multiple sclerosis remains unknown. The study of Kawana et al. in the present issue of the journal might provide a clue to the possible role of NLRP 3 inflammasome in inflammatory demyelination of multiple sclerosis.