A murine DC-SIGN homologue contributes to early host defense against <i>Mycobacterium tuberculosis</i>

Tanne, Antoine; Ma, Bin-Guang; Boudou, Frédéric; Tailleux, Ludovic; Botella, Hélène; Badell, Edgar; Levillain, Florence; Taylor, Maureen E.; Drickamer, Kurt; Nigou, Jérôme; Dobos, Karen M.; Puzo, Germain; Vestweber, Dietmar; Wild, Martin K.; Marcinko, Marie; Sobieszczuk, Peter; Stewart, Lauren; Lebus, Daniel; Gicquel, Brigitte; Neyrolles, Olivier

doi:10.1084/jem.20090188

Cited by 98 publications

(98 citation statements)

References 58 publications

(94 reference statements)

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“…Among the seven murine SIGNR homologs, the absence of SIGNR1, SIGNR3, or SIGNR5 did not hamper survival after M. tuberculosis infection (59,60). In this study, we concentrated on addressing the role of murine mannose receptor and SIGNR1, because SIGNR1 may associate with TLR4/myeloiddifferentiation factor 2 and modulate downstream signaling (39).…”

Section: Discussionmentioning

confidence: 99%

Partial Redundancy of the Pattern Recognition Receptors, Scavenger Receptors, and C-Type Lectins for the Long-Term Control of Mycobacterium tuberculosis Infection

Court

Vasseur

Vacher

et al. 2010

The Journal of Immunology

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Mycobacterium tuberculosis is recognized by multiple pattern recognition receptors involved in innate immune defense, but their direct role in tuberculosis pathogenesis remains unknown. Beyond TLRs, scavenger receptors (SRs) and C-type lectins may play a crucial role in the sensing and signaling of pathogen motifs, as well as contribute to M. tuberculosis immune evasion. In this study, we addressed the relative role and potential redundancy of these receptors in the host response and resistance to M. tuberculosis infection using mice deficient for representative SR, C-type lectin receptor, or seven transmembrane receptor families. We show that a single deficiency in the class A SR, macrophage receptor with collagenous structure, CD36, mannose receptor, specific ICAM-3 grabbing nonintegrin-related, or F4/80 did not impair the host resistance to acute or chronic M. tuberculosis infection in terms of survival, control of bacterial clearance, lung inflammation, granuloma formation, and cytokine and chemokine expression. Double deficiency for the SRs class A SR types I and II plus CD36 or for the C-type lectins mannose receptor plus specific ICAM-3 grabbing nonintegrin-related had a limited effect on macrophage uptake of mycobacteria and TNF response and on the long-term control of M. tuberculosis infection. By contrast, mice deficient in the TNF, IL-1, or IFN-γ pathway were unable to control acute M. tuberculosis infection. In conclusion, we document a functional redundancy in the pattern recognition receptors, which might cooperate in a coordinated response to sustain the full immune control of M. tuberculosis infection, in sharp contrast with the nonredundant, essential role of the TNF, IL-1, or IFN-γ pathway for host resistance to M. tuberculosis.

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Section: Discussionmentioning

confidence: 99%

Partial Redundancy of the Pattern Recognition Receptors, Scavenger Receptors, and C-Type Lectins for the Long-Term Control of Mycobacterium tuberculosis Infection

Court

Vasseur

Vacher

et al. 2010

The Journal of Immunology

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“…Disruption of SIGNR1 signaling (e.g., SOCS1) results in augmented pathogenic conditions, leading to further disequilibrium and lack of a functional homeostasis required for resolving L. m infection. Accordingly, future investigations are warranted to assess the impact of signals directed by SIGNR1 interaction with P. UF1 that mediate regulation during inflammatory conditions and whether mannose-containing S-layer constituents of P. UF1, including lipomannan synthesized by glycolipid pathways involving mannosyltransferases PimA and MptA (94), initiate regulatory signals (SOCS1) in intestinal DCs that skew pathogen-induced inflammation toward regulation.…”

Section: Methodsmentioning

confidence: 99%

Commensal Propionibacterium strain UF1 mitigates intestinal inflammation via Th17 cell regulation

Colliou¹,

Ge²,

Sahay³

et al. 2017

Journal of Clinical Investigation

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“…Therefore DNGR-1 may play a role in adaptive immunity to infections that induce cell death even if it does not act as a PRR. SIGNR3 (CD209d), a mouse CLR that recognizes Mycobacterium tuberculosis and its mannosylated lipoarabinomannan (ManLAM) component, also appears to signal via a hemITAM-Syk pathway that results in induction of proinflammatory cytokines in mouse macrophages (Tanne et al, 2009). Therefore, mouse SIGNR3 might constitute an additional …”

Section: Hemitam Signalingmentioning

confidence: 99%

Myeloid C-type Lectin Receptors in Pathogen Recognition and Host Defense

2011

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C-type lectin receptors (CLRs) comprise a heterogeneous group of transmembrane proteins. Many of them are expressed in myeloid cells and signal in response to pathogen-derived or self ligands to initiate or regulate cell activation. Here, we review the properties of myeloid CLRs, highlighting how their signaling function is coordinated with that of other innate receptor families to control immunity to infection.

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

Cited by 98 publications

References 58 publications

Partial Redundancy of the Pattern Recognition Receptors, Scavenger Receptors, and C-Type Lectins for the Long-Term Control of Mycobacterium tuberculosis Infection

Partial Redundancy of the Pattern Recognition Receptors, Scavenger Receptors, and C-Type Lectins for the Long-Term Control of Mycobacterium tuberculosis Infection

Commensal Propionibacterium strain UF1 mitigates intestinal inflammation via Th17 cell regulation

Myeloid C-type Lectin Receptors in Pathogen Recognition and Host Defense

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