Endotoxin-induced expression of murine bactericidal permeability/increasing protein is mediated exclusively by Toll/IL-1 receptor domain-containing adaptor inducing IFN-β-dependent pathways

被引：29

作者：

Eckert, M ^{[1
]}

Wittmann, I ^{[1
]}

Röllinghoff, M ^{[1
]}

Gessner, A ^{[1
]}

Schnare, M ^{[1
]}

机构：

[1] Univ Erlangen Nurnberg, Inst Clin Microbiol Immunol & Hyg, D-91054 Erlangen, Germany

来源：

JOURNAL OF IMMUNOLOGY | 2006年 / 176卷 / 01期

关键词：

D O I：

10.4049/jimmunol.176.1.522

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Antimicrobial effector proteins are a key mechanism for the innate immune system to combat pathogens once they infect the host. We report the identification and cloning of the mouse homologue of human bactericidal permeability/increasing protein (BPI). Mouse BPI is constitutively expressed in lymphatic organs and tissues as well as in mouse testis. Upon stimulation with different TLR ligands, mouse BPI is strongly expressed in granulocytes and, surprisingly, in bone marrow-derived dendritic cells. Mouse BPI is most strongly induced by bacterial LPS through a signaling pathway that is completely dependent on TLR4-Toll/IL-1R domain-containing adaptor inducing IFN-beta. Functional studies revealed that mouse BPI does have the potential to neutralize LPS and inhibits bacterial growth. Mouse BPI is expressed in granulocytes and bone marrow-derived dendrific cells, and the transcriptional activation is controlled by TLRs.

引用

页码：522 / 528

页数：7

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