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Interleukin-10 genotypes are associated with systemic sclerosis and influence disease-associated autoimmune responses

Genes & Immunity volume 6, pages 274–278 (2005)Cite this article

Abstract

Systemic sclerosis (SSc; scleroderma) is a connective tissue disease, characterized by fibrotic, immunological, and vascular abnormalities. Interleukin-10 (IL-10) is an anti-inflammatory cytokine that modulates collagen production and B-cell survival. To determine if certain IL-10 genotypes are risk factors for the development of SSc and influence disease-associated autoimmune responses, 248 Caucasian and 264 Japanese SSc patients and controls were genotyped for three loci: −3575, −2849, and −2763. Sera from patients were characterized for SSc-associated autoantibodies. In Caucasians, at −3575 and −2763, the frequency of AA homozygotes was higher in patients as compared with controls (P=0.0005; P=0.002). In Japanese subjects, the frequency of AC heterozygotes at −2763 was higher, and that of CC homozygotes lower, in patients with diffuse SSc as compared to controls (P=0.04). Particular IL-10 genotypes were associated with SSc-related autoantibodies. These results suggest that IL-10 genotypes contribute to the etiology of scleroderma.

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Acknowledgements

This work was supported in part by the US Department of Energy cooperative agreement DE-FC09-02CH11109. We are grateful to the study subjects for their blood donation and to the physicians for facilitating the patient participation.

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Authors and Affiliations

  1. Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA

    L L Hudson, K M Rocca & J P Pandey

  2. Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan

    M Kuwana

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  1. L L Hudson
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  2. K M Rocca
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  3. M Kuwana
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  4. J P Pandey
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Correspondence to J P Pandey.

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Hudson, L., Rocca, K., Kuwana, M. et al. Interleukin-10 genotypes are associated with systemic sclerosis and influence disease-associated autoimmune responses. Genes Immun 6, 274–278 (2005). https://doi.org/10.1038/sj.gene.6364180

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