A murine DC-SIGN homologue contributes to early host defense against Mycobacterium tuberculosis

被引：87

作者：

Tanne, Antoine ^{[1
,2
,5
]}

Ma, Bo ^{[3
]}

Boudou, Frederic ^{[2
]}

Tailleux, Ludovic ^{[2
]}

Botella, Helene ^{[1
,5
]}

Badell, Edgar ^{[2
]}

Levillain, Florence ^{[1
,5
]}

Taylor, Maureen E. ^{[4
]}

Drickamer, Kurt ^{[4
]}

Nigou, Jerome ^{[1
,5
]}

Dobos, Karen M. ^{[6
]}

Puzo, Germain ^{[1
,5
]}

Vestweber, Dietmar ^{[7
]}

Wild, Martin K. ^{[7
]}

Marcinko, Marie ^{[3
]}

Sobieszczuk, Peter ^{[3
]}

Stewart, Lauren ^{[3
]}

Lebus, Daniel ^{[3
]}

Gicquel, Brigitte ^{[2
]}

Neyrolles, Olivier ^{[1
,2
,5
]}

机构：

[1] Univ Toulouse 3, Univ Toulouse, Inst Pharmacol & Biol Struct, F-31077 Toulouse, France

[2] Inst Pasteur, Mycobacterial Genet Unit, F-75724 Paris, France

[3] Scripps Res Inst, Dept Physiol Chem, Consortium Funct Glyc, La Jolla, CA 92037 USA

[4] Univ London Imperial Coll Sci Technol & Med, Div Mol Biosci, London SW7 2AZ, England

[5] Univ Toulouse 3, Univ Toulouse, CNRS, F-31077 Toulouse, France

[6] Colorado State Univ, Dept Microbiol Immunol & Pathol, Mycobacteria Res Labs, Ft Collins, CO 80523 USA

[7] Max Planck Inst Mol Biomed, D-48149 Munster, Germany

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2009年 / 206卷 / 10期

基金：

英国惠康基金;

关键词：

C-TYPE LECTINS; TOLL-LIKE RECEPTORS; DENDRITIC CELL; IMMUNE-RESPONSE; MICE LACKING; MOUSE DC; RECOGNITION; INFECTION; DECTIN-1; MACROPHAGES;

D O I：

10.1084/jem.20090188

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The C-type lectin dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) mediates the innate immune recognition of microbial carbohydrates. We investigated the function of this molecule in the host response to pathogens in vivo, by generating mouse lines lacking the DC-SIGN homologues SIGNR1, SIGNR3, and SIGNR5. Resistance to Mycobacterium tuberculosis was impaired only in SIGNR3-deficient animals. SIGNR3 was expressed in lung phagocytes during infection, and interacted with M. tuber-culosis bacilli and mycobacterial surface glycoconjugates to induce secretion of critical host defense inflammatory cytokines, including tumor necrosis factor (TNF). SIGNR3 signaling was dependent on an intracellular tyrosine-based motif and the tyrosine kinase Syk. Thus, the mouse DC-SIGN homologue SIGNR3 makes a unique contribution to protection of the host against a pulmonary bacterial pathogen.

引用

页码：2205 / 2220

页数：16

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