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Interleukin 10 (IL-10) Influences Autoimmune Response in Primary Sjögren's Syndrome and Is Linked to IL-10 Gene Polymorphism

JUAN-MANUEL ANAYA, PAULA A. CORREA, MÓNICA HERRERA, JOYCE ESKDALE, and GRANT GALLAGHER

ABSTRACT.

Objective.
To investigate the association between serum levels of interleukin 10 (IL-10), the synthesis of autoantibodies, salivary gland disease activity, clinical manifestations, and IL-10 microsatellite polymorphism in patients with primary Sjögren's syndrome (pSS).

Methods. Serum IL-10 and autoantibody levels [IgG anti-Ro and anti-La, total and IgA rheumatoid factor (RF)] were measured by ELISA. A minor salivary gland (MSG) biopsy was performed in all patients and the focus score was determined as a measure of salivary gland disease activity. In addition, IL-10 microsatellite typing was performed by polymerase chain reaction technique.

Results. IL-10 concentration was higher in patients (n = 39) than in controls (n = 15) (21.4 ± 6.7 vs 2.5 ± 3.5 pg/ml; p = 0.001). We found a significant positive correlation between IL-10 levels and titers of IgA RF, anti-Ro, and anti-La antibodies, as well as focus score. In comparison with patients with low IL-10 production (< 9.5 pg/ml), patients producing high IL-10 had significantly more episodes of cutaneous vasculitis and a higher proportion of them carried the IL-10.G9 allele.

Conclusion. Autoimmune response in pSS patients as well as salivary gland disease activity and cutaneous involvement appears to be mediated by IL-10 levels; in turn, there is a linkage with IL-10 gene polymorphism. (J Rheumatol 2002;29:1874-6)

Key Indexing Terms:

SJÖGREN'S SYNDROME
INTERLEUKIN 10
ANTI-RO ANTIBODIES
ANTI-LA ANTIBODIES
RHEUMATOID FACTOR
POLYMORPHISM
GENETICS


From the Rheumatology Unit, Corporación para Investigaciones Biológicas (CIB), Clínica Universitaria Bolivariana, School of Medicine, Universidad Pontificia Bolivariana (UPB), Medellin, Colombia, and the Department of Surgery, University of Glasgow, Glasgow Royal Infirmary, Glasgow, Scotland.

Supported by the Corporación para Investigaciones Biológicas, Medellín, Colombia.

J-M. Anaya, MD, Chief, Rheumatology Unit, CIB, and Professor of Medicine, School of Medicine, UPB; P.A. Correa, MSc, Research Assistant; M. Herrera, BSc, Research Assistant, Rheumatology Unit, CIB, and Medical Student, School of Medicine, UPB; J. Eskdale, PhD, Research Assistant; G. Gallagher, PhD, Chief, Genetics Laboratory, Department of Surgery, University of Glasgow, Glasgow Royal Infirmary.

Address reprint requests to Dr. J-M. Anaya, Rheumatology Unit, Corporación para Investigaciones Biológicas, Cra 72-A-78-B-141 Medellín, Colombia. E-mail: jmanaya@epm.net.co

Submitted August 30, 2001; revision accepted February 7, 2002.




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