Lymphocyte apoptosis in systemic lupus erythematosus: relationships with Fas expression, serum soluble Fas and disease activity

Author:

Courtney P A1,Crockard A D2,Williamson K3,McConnell J4,Kennedy R J3,Bell A L2

Affiliation:

1. Department of Rheumatology and Immunology, Royal Victoria Hospital, Belfast; Department of Rheumatology and Immunology, Musgrove Park Hospital, Stockman's Lane, Belfast, BT0 7JB, Ireland

2. Department of Rheumatology and Immunology, Royal Victoria Hospital, Belfast; Arthritis Research Group, Centre for Inflammation and Repair, Musgrave Park Hospital, Belfast

3. Arthritis Research Group, Centre for Inflammation and Repair, Musgrave Park Hospital, Belfast

4. Department of Rheumatology and Immunology, Royal Victoria Hospital, Belfast

Abstract

Lupus specific autoantigens are exposed on apoptotic cells. The increased number of apoptotic lymphocytes reported in systemic lupus erythematosus (SLE) may be attributable to abnormalities of lymphocyte Fas expression or serum soluble Fas. In the present study we analysed the count of circulating apoptotic lymphocytes in SLE patients (n ‘ 50), by flow cytometry using Annexin V, compared to rheumatoid arthritis patients (RA, n ‘ 20), inflammatory bowel disease patients (IBD, n ‘ 20) and normal controls (n ‘ 20). Lymphocyte Fas expression and serum soluble Fas were measured and related to numbers of apoptotic lymphocytes. The percentage of apoptotic lymphocytes, determined by Annexin V binding, was significantly increased in peripheral blood of SLE patients (median ‘ 4.2%) compared with normal healthy donors (median ‘ 1.1%) and IBD patients (median ‘ 2.0%) but not RA (median ‘ 3.9%). SLE lymphocyte Fas expression was not significantly different from RA or IBD patients. Serum soluble Fas in SLE patients correlated positively with apoptotic lymphocytes and antibodies to double stranded DNA. This study suggests that increased apoptotic lymphocytes and increased lymphocyte Fas expression may not be specific to SLE. Serum soluble Fas may have a role in the regulation of lymphocyte apoptosis in SLE.

Publisher

SAGE Publications

Subject

Rheumatology

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