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Erythrocyte C4d and Complement Receptor 1 in Systemic Lupus Erythematosus

VANDANA SINGH, JAMES A. MAHONEY, and MICHELLE PETRI

ABSTRACT.

Objective. Complement activation and ineffective clearance of complement-bearing immune complexes via erythrocytes contribute to the pathogenesis of systemic lupus erythematosus (SLE). Abnormally high levels of erythrocyte C4d and low levels of complement receptor 1 (CD35) have been reported in SLE and might have diagnostic utility. We investigated whether erythrocyte C4d and complement receptor 1 were specific for SLE and whether there was any association with disease activity.

Methods. Expression of complement receptor 1 (CD35) and complement protein C4d on erythrocytes was measured by indirect immunofluorescence and flow cytometry on the same day as the blood draw, in patients with SLE, patients with rheumatic disease, and in normal controls.

Results. Within the SLE population, there was no association with disease activity measured by the physician's global assessment or SELENA SLE Disease Activity Index, nor with past or current lupus nephritis. Assays were not specific for SLE, with higher levels also seen in antiphospholipid syndrome.

Conclusion. Overlap of erythrocyte C4d and CD35 between SLE and other rheumatic diseases limits their utility as diagnostic tests. However, longitudinal investigation of these assays is warranted, especially given the higher levels in some patients with primary antiphospholipid syndrome. (J Rheumatol First Release Aug 15 2008)

Key Indexing Terms:

SYSTEMIC LUPUS ERYTHEMATOSUS
COMPLEMENT


From the Mount Sinai Medical Center, New York, New York; and Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Supported by the Hopkins Lupus Cohort AR 43727 and the Johns Hopkins University Clinical Research Center MOI-RR 00052.

V. Singh, DO, Mount Sinai Medical Center; J.A. Mahoney, PhD; M. Petri, MD, MPH, Johns Hopkins University School of Medicine.

Address reprint requests to Dr. M. Petri, 1830 E. Monument St., Suite 7500, Baltimore, MD 21205. E-mail: mpetri@jhmi.edu

Accepted for publication June 3, 2008.



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