PMID: 9532333Apr 9, 1998Paper

The genetic susceptibility to Graves' disease

Baillière's Clinical Endocrinology and Metabolism
Y Tomer, T F Davies

Abstract

Graves' disease (GD) develops as a result of a complex interaction between genetic susceptibility genes and likely environmental factors. Most epidemiological data support an important genetic contribution to the development of GD. The concordance rate of GD in monozygotic twins is 30-60% and in dizygotic twins 3-9%, and thyroid autoantibodies have been reported in up to 50% of the siblings of patients with GD. For many years now, HLA studies have consistently shown an increased frequency of HLA-DR3 in Caucasian patients with GD; but with only a risk ratio of 3-5. However, recent advances in human genome mapping techniques have enabled the study of many other candidate genes. Of these additional, non-HLA genes, only CTLA-4 has been consistently found to be associated with GD. Using a linkage based approach which only detects highly significant susceptibility genes we have recently reported preliminary results which demonstrated that a marker located approximately 25 cM from the TSH receptor gene on chromosome 14q31 is linked to GD and in the same vicinity as the IDDM-11 locus. Such results, if confirmed, may signal the presence of a gene family related to endocrine autoimmunity on chromosome 14q31.

References

Nov 1, 1977·Acta Endocrinologica·K BechJ H Larsen
Oct 25, 1975·Lancet·R G BaxterL Ryan
Jan 1, 1979·The Journal of Clinical Investigation·N R FaridN D Carter
Dec 1, 1977·Acta Endocrinologica·A KawaT Kanehisa
Dec 1, 1977·The Journal of Clinical Endocrinology and Metabolism·N R FaridR F O'Driscoll
Dec 1, 1977·Clinical Endocrinology·W M TunbridgeP A Smith
Aug 1, 1978·Tissue Antigens·S H ChanJ S Cheah
Sep 30, 1978·British Medical Journal·P P YeoJ S Cheah
Jan 1, 1992·Autoimmunity·A P Weetman
Nov 1, 1992·Human Immunology·R P DongT Sasazuki
Nov 1, 1992·Diabetes·M A PermuttY Tanizawa
Aug 1, 1991·The Journal of Clinical Endocrinology and Metabolism·A MangklabruksL J DeGroot
Jun 1, 1990·Human Immunology·D H Sachs, F H Bach
Jul 1, 1990·Clinical Endocrinology·E Lundgren, S Borup Christensen
Jul 1, 1990·Clinical Endocrinology·N TandonN Kochupillai
Jan 1, 1989·Endocrinology·D S NeufeldT F Davies
Jan 1, 1989·Genetic Epidemiology·H PayamiG Thomson
Dec 1, 1989·Harefuah·J E Zabelle
Oct 1, 1987·The Journal of Clinical Endocrinology and Metabolism·A DemaineN R Farid
Jun 1, 1988·Clinical Endocrinology·A P WeetmanB Shine
Jan 1, 1986·Immunologic Research·A P Weetman
Nov 1, 1986·Clinical Endocrinology·M FreckerN R Farid
Oct 15, 1986·Experientia·K Bender
May 1, 1987·The Journal of Clinical Endocrinology and Metabolism·H TamaiS Nagataki
Jul 1, 1985·Acta Endocrinologica·A P WeetmanA M McGregor
Oct 1, 1985·The Journal of Clinical Endocrinology and Metabolism·V StenszkyN R Farid
Sep 1, 1985·The Journal of Clinical Endocrinology and Metabolism·T F Davies
Jan 1, 1973·Acta Endocrinologica·B S ChertowB L Fariss
Nov 1, 1973·The Journal of Clinical Endocrinology and Metabolism·H H BodeA P Forbes
Feb 25, 1967·British Medical Journal·A J McFadzean, R Yeung
May 24, 1980·Lancet·A M McGregorP J Dewar

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Citations

Jun 30, 2000·Endocrinology and Metabolism Clinics of North America·R S Bahn
Dec 17, 2002·Thyroid : Official Journal of the American Thyroid Association·Pavel PichurinSandra M McLachlan
Mar 24, 2005·Thyroid : Official Journal of the American Thyroid Association·Antonio PetroneRaffaella Buzzetti
Mar 23, 2000·The Journal of Clinical Investigation·S CostagliolaG Vassart
Apr 24, 2012·Journal of Environmental and Public Health·Gerry K Schwalfenberg
Jun 4, 2014·Endocrinology and Metabolism Clinics of North America·Becky T MuldoonHenry B Burch
Dec 13, 2003·Autoimmunity·Gattadahalli S Seetharamaiah
Apr 27, 2000·Endocrine Reviews·L BartalenaC Marcocci
Mar 9, 2002·The Journal of Immunology : Official Journal of the American Association of Immunologists·Yuji NagayamaMasami Niwa
Apr 20, 2013·Allergologia et immunopathologia·Z BrzozaD Moczulski

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