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Analysis of the REL polymorphism rs13031237 in autoimmune diseases
  1. Jezabel Varadé1,
  2. Rogelio Palomino-Morales2,
  3. Norberto Ortego-Centeno3,
  4. Manuel Díaz-Rubio4,
  5. Benjamín Fernández-Gutiérrez5,
  6. Miguel Ángel González-Gay6,
  7. Dora Pascual-Salcedo7,
  8. Alejando Balsa8,
  9. Antonio Iglesias9,
  10. María Gómez-García10,
  11. Torsten Witte11,
  12. Timothy R D J Radstake12,
  13. Marieke J H Coenen13,
  14. Elena Urcelay1,
  15. Javier Martín2
  1. 1Department of Clinical Immunology, Hospital Clínico San Carlos, Madrid, Spain
  2. 2Instituto de Parasitología y Biomedicina “López-Neyra”, CSIC, Granada, Spain
  3. 3Department of Internal Medicine, Hospital Clínico San Cecilio, Granada, Spain
  4. 4Department of Gastroenterology, Hospital Clínico San Carlos, Madrid, Spain
  5. 5Department of Rheumatology, Hospital Clínico San Carlos, Madrid, Spain
  6. 6Rheumatology Unit, Hospital Xeral-Calde, Lugo, Spain
  7. 7Department of Clinical Immunology, Hospital La Paz, Madrid, Spain
  8. 8Department of Rheumatology, Hospital La Paz, Madrid, Spain
  9. 9Universidad Nacional de Colombia, Bogotá, Colombia
  10. 10Department of Gastroenterology, Hospital Virgen de las Nieves, Granada, Spain
  11. 11Medical School Hannover, Hannover, Germany
  12. 12Department of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
  13. 13Department of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
  1. Correspondence to Jezabel Varadé, Department of Clinical Immunology, Hospital Clínico San Carlos, C/Prof Martín Lagos s/n, 1a Sur, 28040 Madrid, Spain; gezabelvarade{at}gmail.com

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REL encodes the c-rel protein, a member of the nuclear factor-κB family of transcription factors involved in the autoimmune response via regulation of the expression of cytokines, anti-apoptotic molecules and cell cycle modulators.1 Expression of c-rel, which is restricted to mature haematopoietic cells, has been described in patients with systemic lupus erythematosus (SLE) and inflammatory bowel disease.2 3 Associations of the REL gene with celiac disease4 and rheumatoid arthritis (RA)5 have been reported. Moreover, Rel knockout mice do not develop autoimmune diseases such as experimental autoimmune encephalomyelitis,6 collagen-induced arthritis or type I diabetes.7

Last year Gregersen et al described the association of the intronic single nucleotide polymorphism (SNP) rs13031237G→T in the REL gene as a risk factor for RA in an expansion of previous genome-wide association …

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