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THU0084 The cd14+/cd16+ monocye subset in rheumatoid arthritis and systemic lupus erythematosus
  1. AP Cairns,
  2. AD Crockard,
  3. AL Bell
  1. Queen’s University Department of Rheumatology, Musgrave Park Hospital, Belfast, UK

Abstract

Background Most human peripheral blood monocytes strongly express surface CD14, and do not express CD16 (CD14++/CD16-). A smaller group of monocytes express lower levels of CD14 and also express CD16 (CD14+/CD16+). This subgroup has different phagocytosing and antigen-presenting capabilities, and is expanded in a number of disease states.1 Monocyte-derived macrophages and dendritic cells have important roles in the pathogenesis of both rheumatoid arthritis and SLE.

Objectives To determine the percentage of circulating CD14+/CD16+ monocytes in rheumatoid arthritis and systemic lupus erythematosus (SLE) and relate this to measures of disease activity and treatment.

Methods Peripheral blood was sampled from 31 SLE patients, 19 rheumatoid arthritis patients and 19 healthy controls. The percentage of CD14+/CD16+ monocytes was determined by immunofluorescence labelling and dual colour flow cytometry.

Results The percentage of CD14+/CD16+ monocytes was significantly reduced in rheumatoid arthritis (median = 4.90%) compared to normal subjects (median = 7.30%, p = 0.014), and in rheumatoid arthritis compared to SLE patients (median = 9.40%, p = 0.009). There was a trend towards a higher percentage of CD14+/CD16+ monocytes in SLE compared to normal subjects, but this did not reach statistical significance. A negative correlation of percentage CD14+/CD16+ monocytes with serum C-reactive protein level was observed (r = – 0.461, p = 0.001). Drug treatment (including corticosteroid dose) did not correlate with the percentage of CD14+/CD16+ monocytes in rheumatoid arthritis or SLE.

Conclusion The percentage of CD14+/CD16+ monocytes in rheumatoid arthritis is lower than in normal subjects and in SLE, and this may contribute to the pathogenesis of rheumatoid arthritis.

Reference

  1. Ziegler-Heitbrock HW. Immunol Today 1996;17(9):424–8

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