Chlamydia muridarum infection elicits a beta interferon response in murine oviduct epithelial cells dependent on interferon regulatory factor 3 and TRIF
about
cPLA2 regulates the expression of type I interferons and intracellular immunity to Chlamydia trachomatisThe toll-Like receptor adaptor TRIF contributes to otitis media pathogenesis and recovery.Induction of interferon-stimulated genes by Chlamydia pneumoniae in fibroblasts is mediated by intracellular nucleotide-sensing receptors.Stimulator of IFN gene is critical for induction of IFN-beta during Chlamydia muridarum infectionMurine mammary carcinoma cells and CD11c(+) dendritic cells elicit distinct responses to lipopolysaccharide and exhibit differential expression of genes required for TLR4 signalingChlamydia-specific CD4 T cell clones control Chlamydia muridarum replication in epithelial cells by nitric oxide-dependent and -independent mechanisms.Analyses of the pathways involved in early- and late-phase induction of IFN-beta during C. muridarum infection of oviduct epithelial cellsRegulation of chlamydial infection by host autophagy and vacuolar ATPase-bearing organelles.Late repression of NF-κB activity by invasive but not non-invasive meningococcal isolates is required to display apoptosis of epithelial cells.Identifying a role for Toll-like receptor 3 in the innate immune response to Chlamydia muridarum infection in murine oviduct epithelial cells.Role of STAT1 in Chlamydia-Induced Type-1 Interferon Production in Oviduct Epithelial Cells.Transcription factor complex AP-1 mediates inflammation initiated by Chlamydia pneumoniae infection.STING-dependent recognition of cyclic di-AMP mediates type I interferon responses during Chlamydia trachomatis infection.Chlamydia trachomatis infection results in a modest pro-inflammatory cytokine response and a decrease in T cell chemokine secretion in human polarized endocervical epithelial cellsCD4+ T cell expression of MyD88 is essential for normal resolution of Chlamydia muridarum genital tract infection.Chlamydia muridarum-specific CD4 T-cell clones recognize infected reproductive tract epithelial cells in an interferon-dependent fashion.Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis.Apoptosis is induced in Chlamydia trachomatis-infected HEp-2 cells by the addition of a combination innate immune activation compounds and the inhibitor wedelolactone.Chlamydia pneumoniae-induced foam cell formation requires MyD88-dependent and -independent signaling and is reciprocally modulated by liver X receptor activation.Lipopolysacchride-treated mammary carcinomas secrete proinflammatory chemokines and exhibit reduced growth rates in vivo, but not in vitro.Toll-like receptor 2 mediates proliferation, survival, NF-kappaB translocation, and cytokine mRNA expression in LIF-maintained mouse embryonic stem cells.
P2860
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P2860
Chlamydia muridarum infection elicits a beta interferon response in murine oviduct epithelial cells dependent on interferon regulatory factor 3 and TRIF
description
2006 nî lūn-bûn
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2006年の論文
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2006年論文
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2006年論文
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2006年論文
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2006年論文
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name
Chlamydia muridarum infection ...... n regulatory factor 3 and TRIF
@ast
Chlamydia muridarum infection ...... n regulatory factor 3 and TRIF
@en
type
label
Chlamydia muridarum infection ...... n regulatory factor 3 and TRIF
@ast
Chlamydia muridarum infection ...... n regulatory factor 3 and TRIF
@en
prefLabel
Chlamydia muridarum infection ...... n regulatory factor 3 and TRIF
@ast
Chlamydia muridarum infection ...... n regulatory factor 3 and TRIF
@en
P2093
P2860
P356
P1476
Chlamydia muridarum infection ...... n regulatory factor 3 and TRIF
@en
P2093
M'hamed Temkit
Micah S Kerr
Raymond M Johnson
Soon-Cheol Hong
Wilbert A Derbigny
P2860
P304
P356
10.1128/IAI.01525-06
P407
P577
2006-12-18T00:00:00Z