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No Association Between Systemic Sclerosis and C77G Polymorphism in the Human PTPRC (CD45) Gene

HOLGER KIRSTEN, MECHTHILD BLUME, FRANK EMMRICH, NICO HUNZELMANN, RUDOLF MIERAU, RITA RZEPKA, PETER VAITH, TORSTEN WITTE, INGA MELCHERS, and PETER AHNERT

ABSTRACT.

Objective. The functional variant C77G (rs17612648) of PTPRC (CD45) was described to confer risk for systemic sclerosis (SSc) in German Caucasians. We analyzed this association in an independent, larger German cohort.

Methods. We genotyped 171 cases and 179 controls. Cases were subgrouped according to sex, autoantibody profiles, or clinical subsets.

Results. No association of SSc with C77G was detected in the whole dataset, in subgroups, or in combined analyses with a previous study.

Conclusion. The results do not confirm PTPRC C77G as a general and independent risk factor for development of SSc. (First Release July 15 2008; J Rheumatol 2008;35:1817-9)

Key Indexing Terms:

SCLERODERMA
SYSTEMIC SCLEROSIS
LEUKOCYTE COMMON ANTIGEN
CD45 ANTIGENS
AUTOIMMUNITY
SINGLE-NUCLEOTIDE POLYMORPHISM


From the Institute of Clinical Immunology and Transfusion Medicine, Center for Biotechnology and Biomedicine (BBZ); and Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig, Leipzig; and Clinical Research Unit for Rheumatology, University Medical Center, Freiburg, Germany.

Supported by grants of the German Federal Ministry for Education and Research: German Network for Systemic Scleroderma to IM, NH, RM; and the Hochschul-Wissenschafts-Programm, the Sächsische Aufbaubank, and the European Fund for Regional Development to PA.

H. Kirsten, MS; M. Blume, MD; F. Emmrich, MD, Institute of Clinical Immunology and Transfusion Medicine, BBZ, University of Leipzig; N. Hunzelmann, MD, Department of Dermatology, University of Cologne, Cologne; R. Mierau, PhD, Rheumaklinik Aachen, Aachen; R. Rzepka, BTA, Clinical Research Unit for Rheumatology, University Medical Center; P. Vaith, MD, Department of Rheumatology and Clinical Immunology, University Medical Center, Freiburg; T. Witte, MD, Department of Clinical Immunology, Center for Internal Medicine, Medical School Hannover, Hannover; I. Melchers, PhD, Clinical Research Unit for Rheumatology, University Medical Center, Freiburg; P. Ahnert, PhD, Institute of Clinical Immunology and Transfusion Medicine, BBZ; Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig.

I. Melchers and P. Ahnert contributed equally to this study.

Address reprint requests to P. Ahnert, University of Leipzig, Institute for Medical Informatics, Statistics and Epidemiology, Haertelstr. 16-18, 04107 Leipzig, Germany. E-mail: peter.ahnert@gmx.net

Accepted for publication April 21, 2008.




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