CD163

CD163 (CD163 Molecule) is a Protein Coding gene. Diseases associated with CD163 include Rosai-Dorfman Disease and Non-Langerhans-Cell Histiocytosis. Among its related pathways are Hematopoietic Stem Cell Differentiation Pathways and Lineage-specific Markers and Binding and Uptake of Ligands by Scavenger Receptors. Gene Ontology (GO) annotations related to this gene include scavenger receptor activity. An important paralog of this gene is CD163L1.

CD163 Molecule

Acute phase-regulated receptor involved in clearance and endocytosis of hemoglobin/haptoglobin complexes by macrophages and may thereby protect tissues from free hemoglobin-mediated oxidative damage. May play a role in the uptake and recycling of iron, via endocytosis of hemoglobin/haptoglobin and subsequent breakdown of heme. Binds hemoglobin/haptoglobin complexes in a calcium-dependent and pH-dependent manner. Exhibits a higher affinity for complexes of hemoglobin and multimeric haptoglobin of HP*1F phenotype than for complexes of hemoglobin and dimeric haptoglobin of HP*1S phenotype. Induces a cascade of intracellular signals that involves tyrosine kinase-dependent calcium mobilization, inositol triphosphate production and secretion of IL6 and CSF1. Isoform 3 exhibits the higher capacity for ligand endocytosis and the more pronounced surface expression when expressed in cells.
After shedding, the soluble form (sCD163) may play an anti-inflammatory role, and may be a valuable diagnostic parameter for monitoring macrophage activation in inflammatory conditions.

Acute-phase response Source: UniProtKB-KW
Negative regulation of inflammatory response to antigenic stimulus Source: Reactome
Receptor-mediated endocytosis Source: Reactome

Secreted; Cell membrane. Isoform 1 and isoform 2 show a lower surface expression when expressed in cells.

Extracellular: 42-1050
Helical: 1051-1071
Cytoplasmic: 1072-1156

A soluble form (sCD163) is produced by proteolytic shedding which can be induced by lipopolysaccharide, phorbol ester and Fc region of immunoglobulin gamma. This cleavage is dependent on protein kinase C and tyrosine kinases and can be blocked by protease inhibitors. The shedding is inhibited by the tissue inhibitor of metalloproteinase TIMP3, and thus probably induced by membrane-bound metalloproteinases ADAMs.
Phosphorylated.