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The aim of the present study was to evaluate levels of soluble CD 163 in sera and fluids from rheumatoid arthritis (RA) patients and elucidate the mechanism that regulates the shedding of CD163. Levels of soluble CD163 in sera and fluids from RA patients were examined by a sandwich enzyme immunoassay and Western blotting. To determine the effects of tissue inhibitors of metalloproteinase (TIMPs) on the shedding of CD163 from monocytes/macrophages, levels of soluble CD163 in cultures of monocytes/macrophages and the expression of CD163 on monocytes/macrophages in the presence or absence of TIMPs were examined by a sandwich enzyme immunoassay and flow cytometry, respectively. The clinical marker that was most associated with serum levels of soluble CD163 was levels of CRP. TIMP-3, but not TIMP-1 or TIMP-2, inhibited the shedding of CD163 from monocytes/macrophages. It was shown that serum levels of soluble CD163 are a sensitive and reliable marker to monitor activated macrophages in synovitis from RA patients and the results imply that the responsible proteinase for the shedding of CD163 is not a member of the matrix metalloproteinases, but is likely to be a member of ADAMs.

Original publication

DOI

10.1046/j.1365-2249.2002.01963.x

Type

Journal article

Journal

Clinical and experimental immunology

Publication Date

10/2002

Volume

130

Pages

156 - 161

Addresses

Department of Immunology and Medical Zoology, School of Medicine, Kagoshima University, Kagoshima City, Japan.

Keywords

Synovial Fluid, Cell Line, Macrophages, Animals, Humans, Spodoptera, Arthritis, Rheumatoid, Autoimmune Diseases, Dexamethasone, Receptors, Cell Surface, Recombinant Fusion Proteins, Tissue Inhibitor of Metalloproteinase-3, Biological Markers, Antigens, CD, Antigens, Differentiation, Myelomonocytic, Transfection, Solubility, Adult, Aged, Middle Aged, Female, Male