Compensatory T cell responses in IRG-deficient mice prevent sustained Chlamydia trachomatis infections
about
The E2-like conjugation enzyme Atg3 promotes binding of IRG and Gbp proteins to Chlamydia- and Toxoplasma-containing vacuoles and host resistance.Guanylate binding proteins promote caspase-11-dependent pyroptosis in response to cytoplasmic LPS.IRG and GBP host resistance factors target aberrant, "non-self" vacuoles characterized by the missing of "self" IRGM proteinsLoss of the interferon-γ-inducible regulatory immunity-related GTPase (IRG), Irgm1, causes activation of effector IRG proteins on lysosomes, damaging lysosomal function and predicting the dramatic susceptibility of Irgm1-deficient mice to infection.Ubiquitin systems mark pathogen-containing vacuoles as targets for host defense by guanylate binding proteinsThe Chlamydia trachomatis Inclusion Membrane Protein CpoS Counteracts STING-Mediated Cellular Surveillance and Suicide Programs.Guanylate binding proteins enable rapid activation of canonical and noncanonical inflammasomes in Chlamydia-infected macrophages.CD4+ T cells develop antiretroviral cytotoxic activity in the absence of regulatory T cells and CD8+ T cells.CD4+ T cells are necessary and sufficient to confer protection against Chlamydia trachomatis infection in the murine upper genital tract.Animal models for studying female genital tract infection with Chlamydia trachomatisChlamydia trachomatis Is Resistant to Inclusion Ubiquitination and Associated Host Defense in Gamma Interferon-Primed Human Epithelial Cells.A CREB3-ARF4 signalling pathway mediates the response to Golgi stress and susceptibility to pathogens.Galectin-3 directs antimicrobial guanylate binding proteins to vacuoles furnished with bacterial secretion systems.Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis.Chlamydia Infection Across Host Species Boundaries Promotes Distinct Sets of Transcribed Anti-Apoptotic Factors.Metabolic crosstalk between host and pathogen: sensing, adapting and competing.Interferon-Inducible GTPases in Host Resistance, Inflammation and Disease.Irgm1 (LRG-47), a regulator of cell-autonomous immunity, does not localize to mycobacterial or listerial phagosomes in IFN-γ-induced mouse cells.
P2860
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P2860
Compensatory T cell responses in IRG-deficient mice prevent sustained Chlamydia trachomatis infections
description
2011 nî lūn-bûn
@nan
2011 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Compensatory T cell responses ...... lamydia trachomatis infections
@ast
Compensatory T cell responses ...... lamydia trachomatis infections
@en
type
label
Compensatory T cell responses ...... lamydia trachomatis infections
@ast
Compensatory T cell responses ...... lamydia trachomatis infections
@en
prefLabel
Compensatory T cell responses ...... lamydia trachomatis infections
@ast
Compensatory T cell responses ...... lamydia trachomatis infections
@en
P2093
P2860
P1433
P1476
Compensatory T cell responses ...... lamydia trachomatis infections
@en
P2093
Amy Rohlfing
Dave C Gondek
Gregory A Taylor
Jörn Coers
Michael N Starnbach
P2860
P304
P356
10.1371/JOURNAL.PPAT.1001346
P50
P577
2011-06-23T00:00:00Z