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Genetic association of Fc receptor-like 3 polymorphisms with autoimmune pancreatitis in Japanese patients
  1. T Umemura1,
  2. M Ota2,
  3. H Hamano3,
  4. Y Katsuyama4,
  5. K Kiyosawa5,
  6. S Kawa6
  1. 1Departments of Internal Medicine, Gastroenterology, and Hepatology, Shinshu University School of Medicine, Matsumoto, Japan
  2. 2Department of Legal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
  3. 3Departments of Internal Medicine, Gastroenterology, and Hepatology, Shinshu University School of Medicine, Matsumoto, Japan
  4. 4Department of Pharmacy, Shinshu University School of Medicine, Matsumoto, Japan
  5. 5Departments of Internal Medicine, Gastroenterology, and Hepatology, Shinshu University School of Medicine, Matsumoto, Japan
  6. 6Departments of Internal Medicine, Gastroenterology, and Hepatology, Shinshu University School of Medicine, Matsumoto, Japan, and Centre for Health, Safety, and Environmental Management, Shinshu University, Matsumoto, Japan
  1. Correspondence to:
    Dr T Umemura
    Department of Internal Medicine, Gastroenterology, and Hepatology, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, 390-8621, Japan; t-ume{at}hsp.md.shinshu-u.ac.jp

https://doi.org/10.1136/gut.2006.095059

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    Autoimmune pancreatitis is characterised by irregular narrowing of the main pancreatic duct, swelling of the pancreas, histological evidence of lymphoplasmacytic inflammation, and high serum immunoglobulin G4 (IgG4) concentration.1–4 Although the human leucocyte antigen DRB1*0405-DQB1*0401 haplotype has been associated with autoimmune pancreatitis,5 the role of genetic factors has not yet been fully defined. A new family of genes called Fc receptor-like genes (FCRLs), which have high structural homology with classical Fcγ receptor genes, has recently been identified.6,7FCRL3 polymorphisms have been shown to be associated with various autoimmune diseases, such as rheumatoid arthritis, autoimmune thyroid disease, and systemic lupus erythematosus, in Japanese populations.8,9 These polymorphisms alter the binding affinity of nuclear factor κB and regulate FCRL3 expression. FCRL3 expression on B cells has been observed in significant amounts and …

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    Footnotes

    • This work was supported in part by Grants-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture of Japan (12670471, 13557047, 15659167 and 16390205) and from the Japan Health Sciences Foundation (KH21022), and by a Research of Specific Diseases, Health and Labour Sciences Research Grant, Japan

    • Conflict of interest: None declared.