Marginal zone macrophages express a murine homologue of DC-SIGN that captures blood-borne antigens in vivo (original) (raw)
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International Immunology, 2003
The marginal zone macrophages of the spleen are implicated in the clearance of polysaccharides, but underlying mechanisms need to be pinpointed. SIGN-R1 is one of ®ve recently identi®ed mouse genes that are homologous to human DC-SIGN and encode a single, external, C-terminal Ctype lectin domain. We ®nd that a polyclonal antibody to a speci®c SIGN-R1 peptide reacts primarily and strongly with a subset of macrophages in the marginal zone of spleen and lymph node medulla. In both sites, SIGN-R1 exists primarily in an aggregated form, resistant to dissociation into monomers upon boiling in SDS under reducing conditions. Upon transfection into three different cell lines, high-mol.-wt forms bearing SIGN-R1 are expressed, as well as reactivity with ER-TR9, a mAb previously described to react selectively with marginal zone macrophages. SIGN-R1-expressing macrophages preferentially sequester dextrans following i.v. injection. Likewise, when phagocytic cells are enriched from spleen and tested in culture, dextran is selectively endocytosed by a subset of very large SIGN-R1 + cells representing~5% of total released macrophages. Uptake of FITC±dextran by these macrophages in vivo and in vitro is blocked by ER-TR9 and polyclonal anti-SIGN-R1 antibodies. Following transfection with SIGN-R1, cell lines become competent to endocytose dextrans. The dextran localizes primarily to compartments lacking transferrin receptor and the LAMP-1 CD107a panlysosomal antigen. Therefore, SIGN-R1 mediates the uptake of dextran polysaccharides, and it is predominantly expressed in the macrophages of the splenic marginal zone and lymph node medulla.
tissues and on specialized macrophages in the placenta and lung. There were no overt differences between DC-SIGN expression in adult and fetal tissues except that DC-SIGN expression in alveolar macrophages was only present after birth. Similarly, in tissues, DC-SIGN was observed primarily on immature (CD83-negative) DCs. Secondly, in the peripheral blood, we found expression of DC-SIGN on a small subset of BDCA-2؉ plasmacytoid DC precursors (pDC2), concordant with our finding of large numbers of DC-SIGN-positive cells in allergic nasal polyps (previously shown to be infiltrated by DC2). Triple-label confocal microscopy indicated that DC-SIGN was colocalized with BDCA-2 and CD123 on DCs in nasal polyp tissue. Consistent with this finding is our observation that DC-SIGN can be up-regulated on monocyte-derived macrophages upon exposure to the Th2 cytokine, IL-13. In summary, our data demonstrate the relevant populations of DC and macrophages that express DC-SIGN in vivo where it may impact the efficiency of virus infection and indicate that DC-SIGN expression may be involved in the Th2 axis of immunity. J. Leukoc. Biol. 71: 445-457; 2002.
Rat Macrophage C-Type Lectin Is an Activating Receptor Expressed by Phagocytic Cells
PLoS ONE, 2013
Macrophage C-type lectin (MCL) is a membrane surface receptor encoded by the Antigen Presenting Lectin-like gene Complex (APLEC). We generated a mouse monoclonal antibody for the study of this receptor in the rat. We demonstrate that rat MCL is expressed on blood monocytes and neutrophils, as well as on several tissue macrophage populations, including alveolar and peritoneal cavity macrophages. We also demonstrate MCL expression on a subset of resident spleen macrophages. Immunohistochemistry analysis of the spleen showed staining specifically in the marginal zone and red pulp. Exposure to pro-inflammatory mediators or to yeast cell wall extract (zymosan) increased surface MCL expression on peritoneal macrophages. We characterized a rat myeloid cell line, RMW, which expresses high levels of MCL. We found that MCL co-immunoprecipitated with the activating adaptor protein FceRIc in these cells. Moreover, beads coated with anti-MCL antibody increased phagocytosis in the RMW cells. Together, these observations indicate that rat MCL is a receptor that activates phagocytosis in myeloid cells under inflammatory conditions. Citation: Lobato-Pascual A, Saether PC, Dahle MK, Gaustad P, Dissen E, et al. (2013) Rat Macrophage C-Type Lectin Is an Activating Receptor Expressed by Phagocytic Cells. PLoS ONE 8(2): e57406.
Marginal zone B cells regulate antigen capture by marginal zone macrophages
Journal of immunology (Baltimore, Md. : 1950), 2011
The marginal zone (MZ) of the mouse spleen contains macrophages that express receptors that trap pathogens, including the scavenger receptor macrophage receptor with a collagenous structure and the C-type lectin specific intracellular adhesion molecule-grabbing nonintegrin receptor 1 (SIGN-R1). We previously reported that expression of SIGN-R1 was decreased in CD19-deficient mice. In this study, we demonstrate that SIGN-R1 is expressed on a subset of macrophage receptor with a collagenous structure (MARCO)(+) macrophages. This subset is diminished when MZ B cells are absent due to either genetic developmental defects or following transient migration of B cells out of the MZ. When B cells return to the MZ, there is a delay in recovery of SIGN-R1-expressing macrophages. During this period, capture of Ficoll, which for the macrophages requires SIGN-R1, remains defective not only by the macrophages, but also by the B cells. Thus, MZ B cells regulate expression of molecules on macrophage...
Blood, 2007
pathogen binding by human myeloid cells related lectin LSECtin mediates antigen capture and − The DC-SIGN http://bloodjournal.hematologylibrary.org/content/109/12/5337.full.html Updated information and services can be found at: (5019 articles) Immunobiology (790 articles) Cell Adhesion and Motility Articles on similar topics can be found in the following Blood collections http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#repub\_requests