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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 1 143-146
Copyright © 1997 by The Endocrine Society

Clinical Studies

CTLA4 Alanine-17 Confers Genetic Susceptibility to Graves’ Disease and to Type 1 Diabetes Mellitus1

Horst Donner, Harald Rau, Paul G. Walfish, Jens Braun, Thorsten Siegmund, Reinhard Finke, Jürgen Herwig, Klaus H. Usadel and Klaus Badenhoop

Medical Department I, Division of Endocrinology, Center of Internal Medicine (H.D., H.R., J.B., J.H., K.H.U., K.B.), and the Department of Pediatrics, Klinikum of the J. W. Goethe University (J.H.), Frankfurt/Main; and the Medical Clinic, Endocrine Department, University Hospital Benjamin Franklin, Free University of Berlin (R.F.), Berlin, Germany; and the Division of Endocrinology and Metabolism and Head and Neck Oncology Program of Mount Sinai Hospital, University of Toronto Medical School, Samuel Lunenfeld Research Institute of Mount Sinai Hospital (P.G.W.), Toronto, Ontario, Canada M5G 1X5

Address all correspondence and requests for reprints to: PD Dr. K. Badenhoop, Medizinische Klinik I, Klinikum der J. W. Goethe University, Theodor-Stern-Kai 7, D-60590 Frankfurt/Main, Germany.

The genetic susceptibility to Graves’ disease and type 1 (insulin-dependent) diabetes mellitus is conferred by genes in the human leukocyte antigen region on the short arm of chromosome 6, but several other genes are presumed to determine disease susceptibility. Among those candidate genes is the cytotoxic T lymphocyte antigen 4 (CTLA4) located on chromosome 2q33 in man. We investigated the distribution of the CTLA4 exon 1 polymorphism (49 A/G) in Graves’ disease and IDDM. This dimorphism at codon 17 results in an amino acid exchange (Thr/Ala) in the leader peptide of the expressed protein and was analyzed by PCR, single strand conformation polymorphism, and restriction fragment length polymorphism analysis in 305 patients with Graves’ disease, 293 patients with IDDM, and 325 controls. Patients with Graves’ disease had significantly more Ala alleles than controls, both as homozygotes (21% vs. 13%) and as heterozygotes (53% vs. 46%), and less Thr as homozygotes (26% vs. 42%; P < 2 x 10-4). The phenotypic frequency of Ala-positive patients (73%) was significantly higher than of controls (58%; P = 10-4; relative risk = 2). Patients with IDDM also had significantly more Ala alleles as homozygotes (19%) or heterozygotes (50%; P = 0.01). In conclusion, an alanine at codon 17 of CTLA4 is associated with genetic susceptibility to Graves’ disease as well as to IDDM.




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