Abstract:
:Macrophages encode several Toll-like receptors (TLRs) that recognize bacterial components, such as lipoproteins (TLR2) or lipopolysaccharides (TLR4), and activate multiple signaling pathways. Activation of transcription factor NF-kappaB by TLR2 or TLR4 signaling promotes proinflammatory and cell survival responses. Alternatively, TLR2 or TLR4 signaling can promote apoptosis if the activation of NF-kappaB is blocked. The gram-negative bacterial pathogen Yersinia pseudotuberculosis secretes into macrophages a protease (YopJ) that inhibits the activation of NF-kappaB and promotes apoptosis. We show that primary macrophages expressing constitutively active inhibitor kappaB kinase beta (IKKbeta) are completely resistant to YopJ-dependent apoptosis, indicating that YopJ inhibits signaling upstream of IKKbeta. Apoptosis is reduced two- to threefold in TLR4(-/-) macrophages infected with Y. pseudotuberculosis, while the apoptotic response of TLR2(-/-) macrophages to Y. pseudotuberculosis infection is equivalent to that of wild-type macrophages. Therefore, TLR4 is the primary source of apoptotic signaling in Yersinia-infected macrophages. Our results also show that a small percentage of macrophages can die as a result of an apoptotic process that is YopJ dependent but does not require TLR2 or TLR4 signaling.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
Zhang Y,Bliska JBdoi
10.1128/iai.71.3.1513-1519.2003keywords:
subject
Has Abstractpub_date
2003-03-01 00:00:00pages
1513-9issue
3eissn
0019-9567issn
1098-5522journal_volume
71pub_type
杂志文章abstract::The kinetics of cytotoxic T lymphocyte antigen 4 (CTLA-4) expression on T cells responding to Cryptococcus neoformans and its role in regulating the T-cell response were examined. Using peripheral blood mononuclear cells stimulated with encapsulated or acapsular C. neoformans we showed that (i) the encapsulated strain...
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doi:10.1128/iai.68.4.2386-2389.2000
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journal_title:Infection and immunity
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doi:10.1128/IAI.63.5.1870-1875.1995
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.67.7.3193-3198.1999
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.34.3.851-855.1981
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journal_title:Infection and immunity
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doi:10.1128/IAI.14.1.95-99.1976
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更新日期:2013-05-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.66.10.5001-5007.1998
更新日期:1998-10-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
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journal_title:Infection and immunity
pub_type: 杂志文章
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journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
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更新日期:1992-05-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
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更新日期:1979-07-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.11.3.441-444.1975
更新日期:1975-03-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.20.2.526-529.1978
更新日期:1978-05-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
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更新日期:2001-04-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.60.12.5267-5282.1992
更新日期:1992-12-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.00756-19
更新日期:2019-12-17 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.19.2.570-574.1978
更新日期:1978-02-01 00:00:00