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Control of the innate immune response by the mevalonate pathway.

Abstract：

:Deficiency in mevalonate kinase (MVK) causes systemic inflammation. However, the molecular mechanisms linking the mevalonate pathway to inflammation remain obscure. Geranylgeranyl pyrophosphate, a non-sterol intermediate of the mevalonate pathway, is the substrate for protein geranylgeranylation, a protein post-translational modification that is catalyzed by protein geranylgeranyl transferase I (GGTase I). Pyrin is an innate immune sensor that forms an active inflammasome in response to bacterial toxins. Mutations in MEFV (encoding human PYRIN) result in autoinflammatory familial Mediterranean fever syndrome. We found that protein geranylgeranylation enabled Toll-like receptor (TLR)-induced activation of phosphatidylinositol-3-OH kinase (PI(3)K) by promoting the interaction between the small GTPase Kras and the PI(3)K catalytic subunit p110δ. Macrophages that were deficient in GGTase I or p110δ exhibited constitutive release of interleukin 1β that was dependent on MEFV but independent of the NLRP3, AIM2 and NLRC4 inflammasomes. In the absence of protein geranylgeranylation, compromised PI(3)K activity allows an unchecked TLR-induced inflammatory responses and constitutive activation of the Pyrin inflammasome.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Akula MK,Shi M,Jiang Z,Foster CE,Miao D,Li AS,Zhang X,Gavin RM,Forde SD,Germain G,Carpenter S,Rosadini CV,Gritsman K,Chae JJ,Hampton R,Silverman N,Gravallese EM,Kagan JC,Fitzgerald KA,Kastner DL,Golenbock DT,Ber

doi

10.1038/ni.3487

subject

Has Abstract

pub_date

2016-08-01 00:00:00

pages

922-9

issue

8

eissn

1529-2908

issn

1529-2916

pii

ni.3487

journal_volume

17

pub_type

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