Abstract
The mannose receptor is a member of the C-type lectin (CLEC) family, which can bind and internalize a variety of endogenous and pathogen-associated ligands. Because of these properties, its role in endocytosis as well as antigen processing and presentation has been studied intensively. Recently, it became clear that the mannose receptor can directly influence the activation of various immune cells. Cell-bound mannose receptor expressed by antigen-presenting cells was indeed shown to drive activated T cells towards a tolerogenic phenotype. On the other hand, serum concentrations of a soluble form of the mannose receptor have been reported to be increased in patients suffering from a variety of inflammatory diseases and to correlate with severity of disease. Interestingly, we recently demonstrated that the soluble mannose receptor directly promotes macrophage proinflammatory activation and trigger metaflammation. In this review, we highlight the role of the mannose receptor and other CLECs in regulating the activation of immune cells and in shaping inflammatory responses.
Highlights
The mannose receptor (MR), termed CD206, is a member of the C-type lectin (CLEC) family
Recent advances have made clear that the MR can actively shape immune responses by directly regulating immune cell activity [11, 73, 77]
The membrane-bound MR has been shown to induce T cell tolerance, whereas the sMR stimulates an inflammatory response in macrophages, both via inhibition of CD45
Summary
The mannose receptor (MR), termed CD206, is a member of the C-type lectin (CLEC) family. Members of this family contain C-type lectin domains (CTLDs), which play an important function in ligand recognition. Type II transmembrane CLECs can bear signaling motives at their cytosolic tail (Figure 1). The MR is mainly expressed by subpopulations of macrophages, immature dendritic cells (DCs) and endothelial cells [1, 2]. Its expression level varies upon the situation and can be differentially regulated by cytokines (e.g. IL-10, IL-4, IL-13 and IFNg), prostaglandins, LPS and the transcription factor PPAR-g [3,4,5,6,7]. Frontiers in Immunology | www.frontiersin.org van der Zande et al
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