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Monocyte receptor function in patients with rheumatoid arthritis
Arthritis and Rheumatism
|October 1, 1981
Summary
Monocytes from rheumatoid arthritis (RA) patients show enhanced Fc receptor function, specifically in E-rosette formation and phagocytosis. Corticosteroid treatment in RA patients significantly reduced this enhanced function, suggesting receptor modulation.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation.
- Monocytes play a crucial role in the immune response and inflammation.
- Fc and C3 receptors on monocytes are involved in immune complex recognition and phagocytosis.
Purpose of the Study:
- To investigate potential abnormalities in Fc and C3 receptor function of monocytes in patients with rheumatoid arthritis (RA) and osteoarthritis (OA).
- To compare monocyte receptor function between active RA patients, OA patients, and healthy volunteers.
- To assess the impact of corticosteroid treatment on monocyte Fc receptor function in RA patients.
Main Methods:
- Monocytes were isolated from patients with active RA, OA, and normal volunteers.
- Fc receptor (FcR) function was assessed by measuring E-rosette (EA) formation and EA phagocytosis.
- C3 receptor (C3R) function was evaluated by binding of EAC (complement-coated erythrocytes) and uptake of iodinated aggregated gamma globulin.
Main Results:
- Monocytes from the majority of active RA patients exhibited enhanced EA-rosette formation and EA phagocytosis compared to normal volunteers and OA patients.
- No significant differences in EAC binding or aggregated gamma globulin uptake were observed among the three groups, indicating specific FcR modulation.
- Corticosteroid-treated RA patients showed a significant depression in EA-rosette formation and phagocytosis, suggesting a modulatory effect of treatment.
Conclusions:
- Monocytes from patients with active rheumatoid arthritis display enhanced Fc receptor-mediated functions.
- These findings suggest a modulation of Fc receptor function in monocytes from RA patients.
- Corticosteroid therapy appears to suppress the enhanced Fc receptor function observed in RA monocytes.