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Increase of soluble FcgRIIIa derived from natural killer cells and macrophages in plasma from patients with rheumatoid arthritis
OBJECTIVE: FcgRIII (CD16), one of the low affinity IgG Fc receptors, is found in 2 alternative forms, a transmembrane FcgRIIIa expressed on natural killer (NK) cells and macrophages, and a glycosylphosphatidylinositol-linked FcgRIIIb present on neutrophils. Both FcgRIII are released from the cell su...
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Published in: | Journal of rheumatology 2003-09, Vol.30 (9), p.1911-1917 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | OBJECTIVE: FcgRIII (CD16), one of the low affinity IgG Fc receptors, is found in 2 alternative forms, a transmembrane FcgRIIIa
expressed on natural killer (NK) cells and macrophages, and a glycosylphosphatidylinositol-linked FcgRIIIb present on neutrophils.
Both FcgRIII are released from the cell surface by proteolytic cleavage and these soluble forms (sFcgRIII) are present in
plasma. Since NK cells and macrophages will be activated locally, leading to shedding of FcgRIIIa and its subsequent release
into blood, we investigated whether sFcgRIIIa plasma concentrations would be a good marker for disease activity in patients
with rheumatoid arthritis (RA). METHODS: We measured sFcgRIIIa with an immuno-PCR in plasma of NA(1+,2-) phenotyped donors.
In this assay, we used CD16 GRM1, which recognizes NA2-FcgRIIIb and FcgRIIIa. We also analyzed precipitated sFcgRIIIa derived
from plasma with immunoblotting with CD16 CLB-LM6.30. RESULTS: The concentration of sFcgRIIIa in patients with RA was about
3 times higher than in healthy controls. In controls, the sFcgRIIIa levels in plasma correlated with the number of NK cells
in peripheral blood. In RA patients, sFcgRIIIa levels were increased directly proportionally to the concentrations of IgG,
IgA, or IgM and to erythrocyte sedimentation rate or Lansbury Index. The electrophoretic mobility of plasma sFcgRIIIa corresponded
with sFcgRIIIa derived from NK cells and/or macrophages. In general, plasma sFcgRIIIa originated from both cell types; however,
the ratio of sFcgRIIIaNK to sFcgRIIIaMf varied in the RA patients. CONCLUSION: Increased sFcgRIIIa levels in RA patients were
found to be caused by NK cell and/or macrophage activation. Plasma sFcgRIIIa levels may serve as a marker for disease activity
in RA. |
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ISSN: | 0315-162X 1499-2752 |