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Characterization of the murine macrophage mannose receptor: demonstration
that the downregulation of receptor expression mediated by interferon-gamma
occurs at the level of transcription
N Harris, M Super, M Rits, G Chang and RA Ezekowitz
Division of Hematology/Oncology, Children's Hospital, Boston, MA 02115.
The macrophage mannose receptor (MMR) is a 175-Kd cell-surface
transmembrane glycoprotein that is expressed on tissue macrophages where it
functions both to mediate the uptake of mannose-rich glycoproteins and as a
phagocytic receptor for bacteria, yeasts, and other pathogenic
microorganisms. In this report we describe the cloning of the full-length
cDNA of the mouse macrophage mannose receptor and we investigate the level
at which interferon gamma (IFN-gamma) downregulates mannose receptor
expression. The latter is a marker of the functional state of the cell as
high levels are expressed on resident and inflammatory macrophages, whereas
cells activated by treatment with IFN-gamma have decreased-to-absent
cell-surface mannose receptor expression. The murine MMR cDNA contains an
open reading frame that predicts a protein of 1,456 amino acids. Transient
expression of the protein in heterologous cells shows that this cDNA
encodes a functional mannose receptor. The deduced amino acid sequence of
this protein has an overall 82% homology with the human mannose receptor
and as such, the ectodomain contains an N-terminus that is cysteine-rich
followed by a fibronectin type II domain and eight carbohydrate recognition
domains (CRDs). The ectodomain is linked to a hydrophobic transmembrane
region and a 46-amino acid cytoplasmic tail. All of the eight CRDs are
particularly well conserved, especially CRD4, which shows 92% homology with
the equivalent region of the human protein. Steady-state levels of murine
MMR mRNA were measured in the macrophage cell line J774E, which is known to
express the protein at the cell surface. These levels were decreased by a
4- to 8-hour incubation with IFN-gamma, but were almost abolished by
overnight treatment with this cytokine. Nuclear run-on experiments showed
that IFN-gamma inhibits MMR gene transcription. Therefore, the regulation
of mannose receptor expression by IFN-gamma provides a novel system in
which to study the mechanisms by which this cytokine represses gene
expression.
Volume 80,
Issue 9,
pp. 2363-2373,
11/01/1992
Copyright © 1992 by The American Society of Hematology
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