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Lupus, Vol. 7, No. 2,
113-118 (1998)
DOI: 10.1191/096120398678919804
High levels of circulating early apoptic peripheral blood mononuclear cells in systemic lupus erythematosus
A Perniok
F Wedekind
Department of Rheumatology, Heinrich-Heine University, Moorenstr. 5, D-40225 Düsseldorf
M Herrmann
Institute of Clinical Immunology, Friedrich - Alexander University, Glückstr. 4a, D-91054 Erlangen, Germany
C Specker
M Schneider
Department of Rheumatology, Heinrich-Heine University, Moorenstr. 5, D-40225 Düsseldorf
Increased in vitro apoptosis and altered expression of apoptosis-related molecules have been reported in systemic lupus erythematosus (SLE). It was speculated that autoantigens released from apoptizing cells may contribute to the etiopathogenesis of SLE by both activation of autoreactive lymphocytes and the formation of immune complexes. Conflicting data about the level of cellular apoptosis from animal models for SLE and human SLE indicate different pathomechanisms.
In the present study we analysed the count of circulating early apoptotic cells and its correlation with the clinical activity in SLE compared with the amount in primary systemic vasculitis (PSV). The percentage of early apoptotic cells determined by Annexin V-FITC binding cells was significantly increased in peripheral blood of SLE patients compared with normal healthy donors (NHD) and PSV (NHD 5.62%, SLE 13.68%, PSV 8.69%). Analysis of lymphocytes revealed significantly increased counts in the T cell populations (NHD 5.15%, SLE 12.22%, PSV 10.01%), whereas the increase in B cells did not reach significance level (NHD 9.20%, SLE 18.95%, PSV 16.59%). Apoptotic cell count revealed no correlation to SLAM-Score or to immunosuppressive therapy, corticosteroid-dosage or absolute lymphocyte count.
The general increase of circulating apoptotic cells may indicate an impaired clearance in SLE patients, independent of clinical activity or therapeutic interventions. Autoantigens from apoptotic cells may contribute to both activation of autoreactive lymphocytes and formation of immune complexes.
Key Words: SLE • apoptosis • autoantigens • lymphocytes • tolerance
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