In:
PLOS Pathogens, Public Library of Science (PLoS), Vol. 18, No. 11 ( 2022-11-30), p. e1010989-
Abstract:
The mediator of IRF3 activation (MITA, also named STING) is critical for immune responses to abnormal cytosolic DNA and has been considered an important drug target in the clinical therapy of tumors and autoimmune diseases. In the present study, we report that MITA undergoes DDOST-mediated N-glycosylation in the endoplasmic reticulum (ER) upon DNA viral infection. Selective mutation of DDOST-dependent N-glycosylated residues abolished MITA oligomerization and thereby its immune functions. Moreover, increasing the expression of Ddost in the mouse brain effectively strengthens the local immune response to herpes simplex virus-1 (HSV-1) and prolongs the survival time of mice with HSV encephalitis (HSE). Our findings reveal the dependence of N-glycosylation on MITA activation and provide a new perspective on the pathogenesis of HSE.
Type of Medium:
Online Resource
ISSN:
1553-7374
DOI:
10.1371/journal.ppat.1010989
DOI:
10.1371/journal.ppat.1010989.g001
DOI:
10.1371/journal.ppat.1010989.g002
DOI:
10.1371/journal.ppat.1010989.g003
DOI:
10.1371/journal.ppat.1010989.g004
DOI:
10.1371/journal.ppat.1010989.g005
DOI:
10.1371/journal.ppat.1010989.g006
DOI:
10.1371/journal.ppat.1010989.g007
DOI:
10.1371/journal.ppat.1010989.s001
DOI:
10.1371/journal.ppat.1010989.s002
DOI:
10.1371/journal.ppat.1010989.s003
DOI:
10.1371/journal.ppat.1010989.s004
DOI:
10.1371/journal.ppat.1010989.s005
DOI:
10.1371/journal.ppat.1010989.s006
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2205412-1
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