Abstract | OBJECTIVE: METHODS: RESULTS: Influx and activation of inflammatory cells (MRP expression) during ICA was decreased in Fc gamma RIII-deficient mice and enhanced in mice lacking Fc gamma RII. Mild cartilage destruction reflected by loss of PGs was consistent with the degree of inflammation. Mice lacking Fc gamma RIII showed almost no PG depletion, whereas in Fc gamma RII(-/-) mice, PG depletion was increased 3-7-fold in various cartilage areas. Initiation of erosive cartilage destruction, as reflected by MMP-mediated VDIPEN expression, was reduced in Fc gamma RIII(-/-) and Fc gamma RI(-/-) mice, directing the two different critical steps of cellular influx and subsequent activation. These aspects were enhanced in Fc gamma RII(-/-) mice. In Fc gamma RI(-/-) and Fc gamma RIII(-/-) mice, VDIPEN expression was 90-99% lower, whereas in Fc gamma RII(-/-) mice, VDIPEN expression was increased 4-fold. Chondrocyte death was reduced in Fc gamma RIII(-/-) mice (68% lower) and enhanced in Fc gamma RII(-/-) mice (6-12-fold higher). Progression of arthritis and erosion of the cartilage surface were markedly elevated in Fc gamma RII(-/-) arthritic joints. CONCLUSION:
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Authors | K C A M Nabbe, A B Blom, A E M Holthuysen, P Boross, J Roth, S Verbeek, P L E M van Lent, W B van den Berg |
Journal | Arthritis and rheumatism
(Arthritis Rheum)
Vol. 48
Issue 1
Pg. 255-65
(Jan 2003)
ISSN: 0004-3591 [Print] United States |
PMID | 12528127
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antigen-Antibody Complex
- Receptors, IgG
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Topics |
- Animals
- Antigen-Antibody Complex
(immunology)
- Arthritis
(immunology, pathology)
- Cartilage
(immunology, pathology)
- Cell Death
- Chondrocytes
(pathology)
- Gene Expression
(immunology)
- Immunophenotyping
- Knee Joint
(immunology, pathology)
- Macrophages
(immunology, pathology)
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Receptors, IgG
(antagonists & inhibitors, genetics)
- Severity of Illness Index
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