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Rheumatology Advance Access originally published online on June 15, 2004
Rheumatology 2004 43(8):965-968; doi:10.1093/rheumatology/keh211
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Rheumatology Vol. 43 No. 8 © British Society for Rheumatology 2004; all rights reserved

Paper

Quantification of fetal microchimeric cells in clinically affected and unaffected skin of patients with systemic sclerosis

H. H. B. Sawaya, S. A. Jimenez and C. M. Artlett

Department of Medicine, Division of Rheumatology, Thomas Jefferson University, 233 S 10th Street, Rm 509 BLSB, Philadelphia, PA 19107, USA.

Correspondence to: C. M. Artlett. E-mail: Carol.Artlett{at}Jefferson.edu

Objective. Fetal microchimerism has been hypothesized as a potential pathogenic mechanism for systemic sclerosis (SSc). This hypothesis was based on the clinical similarities between SSc and graft-vs-host disease and the identification of microchimeric cells in affected SSc tissues. The aim of this study was to compare the quantity of microchimeric cells in clinically affected and non-affected skin of female patients with SSc.

Methods. Fluorescence in situ hybridization (FISH) and real-time PCR were employed in paired skin biopsies obtained from clinically affected and unaffected areas from five female SSc patients with diffuse cutaneous SSc (dcSSC) and 10 healthy women. All women in the study had delivered a male fetus.

Results. FISH analysis revealed the presence of male fetal cells in 1/5 SSc patients (20.0%) compared with 0/10 healthy women (P = 0.0037), whereas quantification by real-time PCR revealed that all SSc samples were positive for male DNA compared with none of the controls. In the five patients with dcSSc, there were similar numbers of microchimeric cells in both affected and unaffected skin (P = 0.4)

Conclusion. The presence of higher numbers of microchimeric cells in clinically unaffected SSc skin, before any clinically detectable evidence of sclerotic changes, suggests that an influx of microchimeric cells may precede the development of tissue fibrosis. This provides additional support to the hypothesis that fetal microchimerism may play a role in the pathogenesis of SSc.

KEY WORDS: Microchimerism, Systemic sclerosis, Affected skin, Unaffected skin, Diffuse


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