Inactivation of inflammasomes by pathogens regulates inflammation


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Inflammatory response is initiated and sustained by the action of quintessential pro-inflammatory cytokines of immune system namely IL-1β and IL-18. The maturation process of those cytokines is ensured by caspase-1 enzymatic activity, that is in turn is tightly controlled by multiprotein complexes called inflammasomes. Inflammasomes are activated in cells of innate immune system in response to recognition of conservative parts of microbes (pathogen-associated molecular patterns) or by sensing molecular signs of tissue damage (damage-associated molecular patterns). Inflammasome activation apart of cytokines secretion leads to pro-inflammatory cell death, so-called pyroptosis. That culminates in release of cytoplasmatic content of cells including cytokines and alarmins that boost immune response against pathogens, as well as pyroptosis destroys replicative niches of intracellular pathogens. During co-evolution with the host, bacterial and viral pathogens developed a range of molecular inhibitors targeting each step of inflammasome activation. In current review, we will discuss the latest knowledge of inflammasomes’ signaling pathways and tricks that pathogens use to avoid immune recognition and clearance. Our better understanding of inflammasome inhibition by pathogens can lead to better therapeutic approaches for the treatment of infectious diseases.

作者简介

F. Garib

Biological Faculty; Department of Immunology; Department of Immunology

编辑信件的主要联系方式.
Email: fgarib@yandex.ru
俄罗斯联邦, Moscow, 119991; Moscow, 123995; Moscow, 119991

A. Rizopulu

Committee on Science and High Technologies

Email: fgarib@yandex.ru
俄罗斯联邦, Moscow, 103265

A. Kuchmiy

Inflammation Research Center, VIB; Department of Internal Medicine

Email: fgarib@yandex.ru
比利时, Zwijnaarde, B-9052; Ghent, B-9000

V. Garib

Department of Pathophysiology and Allergy Research

Email: fgarib@yandex.ru
奥地利, Vienna, 1090


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