Association of Fc receptor-like 5 (FCRL5) with Graves' disease is secondary to the effect of FCRL3

• Published in: Clinical endocrinology (Oxford) Vol. 73; no. 5; pp. 654 - 660
• Main Authors: Simmonds, Matthew J., Brand, Oliver J., Barrett, Jeffrey C., Newby, Paul R., Franklyn, Jayne A., Gough, Stephen C.L.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.11.2010; Blackwell; Wiley Subscription Services, Inc; Wiley
• Subjects: Biological and medical sciences; Case-Control Studies; Endocrinopathies; European Continental Ancestry Group - genetics; Fundamental and applied biological sciences. Psychology; Genetic Predisposition to Disease; Graves Disease - genetics; Humans; Linkage Disequilibrium; Logistic Models; Medical sciences; Middle Aged; Non tumoral diseases. Target tissue resistance. Benign neoplasms; Polymorphism, Single Nucleotide; Receptors, Cell Surface - genetics; Receptors, Fc; Receptors, Immunologic - genetics; Thyroid. Thyroid axis (diseases); Vertebrates: endocrinology; Endocrinopathy; Immunopathology; Association; Hyperthyroidism; Thyroid diseases; Immunoglobulin receptor; Secondary effect; Graves disease; Autoimmune disease; Endocrinology; Medicine

Summary Objective  The Fc receptor‐like 3 (FCRL3) molecule, involved in controlling B‐cell signalling, may contribute to the autoimmune disease process. Recently, a genome‐wide screen detected association of neighbouring gene FCRL5 with Graves’ disease (GD). To determine whether FCRL5 represents a f...