Brief Article
Copyright ©2010 Baishideng. All rights reserved
World J Gastroenterol. Jan 21, 2010; 16(3): 354-358
Published online Jan 21, 2010. doi: 10.3748/wjg.v16.i3.354
Immunogenetic characteristics of patients with autoimmune gastritis
Aino Mirjam Oksanen, Katri Eerika Haimila, Hilpi Iris Kaarina Rautelin, Jukka Antero Partanen
Aino Mirjam Oksanen, Herttoniemi Hospital, Health Centre, City of Helsinki, PO Box 6300, 00099 Helsinki, Finland
Katri Eerika Haimila, Finnish Red Cross Blood Service, Clinical Laboratory, 00310 Helsinki, Finland
Hilpi Iris Kaarina Rautelin, Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, 00014 Helsinki, Finland; HUSLAB, Helsinki University Central Hospital, 00029 Helsinki, Finland; Department of Medical Sciences, University and University Hospital of Uppsala, 75185 Uppsala, Sweden
Jukka Antero Partanen, Finnish Red Cross Blood Service, Research and Development, 00310 Helsinki, Finland
Author contributions: Oksanen AM designed the study, enrolled patients, and wrote the manuscript; Haimila KE performed the immunogenetic studies; Rautelin HIK analyzed the data and revised the manuscript; Partanen JA designed and analyzed the immunogenetic studies.
Supported by A grant from the Research Unit of the Health Centre, City of Helsinki
Correspondence to: Aino Mirjam Oksanen, MD, Herttoniemi Hospital, Health Centre, City of Helsinki, PO Box 6300, 00099 Helsinki, Finland. aino.oksanen@hel.fi
Telephone: +358-9-3105511 Fax: +358-9-31055894
Received: September 25, 2009
Revised: November 14, 2009
Accepted: November 21, 2009
Published online: January 21, 2010
Abstract

AIM: To explore whether predisposition to autoimmune gastritis (AIG) is found in human leukocyte antigen (HLA), cytokine or killer cell immunoglobulin-like receptor (KIR) gene variations.

METHODS: Twelve Finnish patients with autoimmune-type severe atrophy of the gastric corpus were included. The patients’ serum was analyzed for pepsinogen I and Helicobacter pylori (H. pylori) antibodies. DNA was separated and the patients were genotyped for HLA-A, B, Cw, DRB1 and DQB1 antigens, and studied for single nucleotide polymorphisms for the following cytokines: interleukin (IL)-1 gene cluster, IL-2, IL-4, IL-6, IL-10, IL-12, interferon γ, transforming growth factor β, and tumor necrosis factor α. Variation in KIR genes was also explored. The results were compared with prevalence of the polymorphisms in Finnish or European populations.

RESULTS: All patients had pepsinogen I levels below normal (mean: 11 μg/L, range: < 5 to 25 μg/L). Three patients had elevated H. pylori IgG antibodies, while H. pylori serology was negative in the rest of the patients. AIG patients carried significantly more often HLA-DRB1*04 (58%) and DQB1*03 (83%) than the general Finnish population did (28% and 51%, respectively; P = 0.045 and 0.034 by the Fisher’s exact test). No patient was positive for HLA-B8-DRB1*03, a well-established autoimmune marker. Neither cytokine polymorphisms nor KIR gene variation showed association with AIG.

CONCLUSION: As explored with modern DNA-based methods, HLA-DRB1*04 and DQB1*03 alleles, but not HLA-B8-DRB1*03, may predispose to AIG.

Keywords: Atrophic gastritis; Autoimmune diseases; Cytokines; Genetic polymorphisms; Human leukocyte antigens; Killer cell immunoglobulin-like receptor