The physiological role of DC-SIGN: A tale of mice and men

García-Vallejo, Juan J.; Kooyk, Yvette van

doi:10.1016/j.it.2013.03.001

Cited by 164 publications

(168 citation statements)

References 45 publications

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“…MMR and DC-SIGN bind both mannose and fucose residues, whereas CLEC10A specifically recognizes a-and b-linked N-acetylgalactosamine. [26][27][28] Each of these carbohydrate structures is present in FX, 29 providing a rationale for a potential interaction between FX and these receptors. However, despite their evident expression in THP1 macrophages (supplemental Figure 1), no colocalization was found when assessed via Duolink-PLA analysis (Figure 2).…”

Section: Discussionmentioning

confidence: 99%

Macrophage receptor SR-AI is crucial to maintain normal plasma levels of coagulation factor X

Muczynski

Bazaa

Loubière

et al. 2016

Blood

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Key Points• SR-AI is the major receptor of FX at the macrophage surface.• Macrophages use SR-AI to control FX circulatory levels.Beside its classical role in the coagulation cascade, coagulation factor X (FX) is involved in several major biological processes including inflammation and enhancement of virusinduced immune responses. We recently reported that the long circulatory half-life of FX is linked to its interaction with liver-resident macrophages. Importantly, we now observed that macrophages, but not undifferentiated monocytes, support this interaction. Using cell biology approaches with primary and THP1-derived macrophages as well as transfected cells, we further identified the scavenger receptor type A member I (SR-AI) to be a macrophage-specific receptor for FX. This result was confirmed using SR-AI-deficient mice, which exhibit reduced circulating levels of FX in vivo and loss of FX-macrophage interactions in vitro. Binding studies using purified proteins revealed that FX binds specifically (half-maximal binding, 3 mg/mL) to the extracellular domain of SR-AI. Altogether, we demonstrate that macrophages regulate FX plasma levels in an SR-AI-dependent manner. (Blood. 2016;127(6):778-786)

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Section: Discussionmentioning

confidence: 99%

Macrophage receptor SR-AI is crucial to maintain normal plasma levels of coagulation factor X

Muczynski

Bazaa

Loubière

et al. 2016

Blood

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“…DC-SIGN/CD209 and MR/CD206 are the 2 lectins able to bind mannosylated FL BCR in vitro 16 and have been described on dendritic cells and macrophages within normal lymphoid tissues. 20,21 We decided to check for their expression within the FL cell niche. First, we highlighted, by flow cytometry, 25 an overexpression of DC-SIGN on CD3/CD19/CD335 Figure 6).…”

Section: Dc-sign Expression Within Fl Lymph Nodesmentioning

confidence: 99%

“…Concerning BCR ligands, both DC-SIGN and MR are expressed by various myeloid cell subsets. 20,21 Interestingly, a high number of tumor-associated macrophages (TAMs) have an adverse prognostic value in FL patients treated with conventional chemotherapy. [22][23][24] …”

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confidence: 99%

DC-SIGN–expressing macrophages trigger activation of mannosylated IgM B-cell receptor in follicular lymphoma

Amin

Mourcin

Uhel

et al. 2015

Blood

113

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“…[17][18][19] As no functional homolog of DC-SIGN exists in mice, 20 we generated humanized mice expressing human DC-SIGN (hSIGN) on conventional DCs. 21 Importantly, delivery of antigens via anti-DC-SIGN monoclonal antibodies (aDC-SIGN) enhances T cell responses in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

Antigen targeting to dendritic cells combined with transient regulatory T cell inhibition results in long-term tumor regression

et al. 2014

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C regulatory T cells (Tregs), resulting in defective T cell priming and failure to induce tumor regression. To circumvent these problems we evaluated a novel combinatorial therapeutic strategy. We show that tumor antigen targeting to DC-SIGN in humanized hSIGN mice via glycans or specific antibodies induces superior T cell priming. Next, this targeted therapy was combined with transient Foxp3 C Treg depletion employing hSIGNxDEREG mice. While Treg depletion alone slightly delayed B16-OVA melanoma growth, only the combination therapy instigated long-term tumor regression in a substantial fraction of mice. This novel strategy resulted in optimal generation of antigen-specific activated CD8C T cells which accumulated in regressing tumors. Notably, Treg depletion also allowed the local appearance of effector T cells specific for endogenous B16 antigens. This indicates that antitumor immune responses can be broadened by therapies aimed at controlling Tregs in tumor environments. Thus, transient inhibition of Treg-mediated immune suppression potentiates DC targeted antigen vaccination and tumor-specific immunity.

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The physiological role of DC-SIGN: A tale of mice and men

Cited by 164 publications

References 45 publications

Macrophage receptor SR-AI is crucial to maintain normal plasma levels of coagulation factor X

Macrophage receptor SR-AI is crucial to maintain normal plasma levels of coagulation factor X

DC-SIGN–expressing macrophages trigger activation of mannosylated IgM B-cell receptor in follicular lymphoma

Antigen targeting to dendritic cells combined with transient regulatory T cell inhibition results in long-term tumor regression

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