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International Immunology Advance Access originally published online on August 13, 2007
International Immunology 2007 19(9):1135-1144; doi:10.1093/intimm/dxm087
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Two genetic loci independently confer susceptibility to autoimmune gastritis

Desmond K. Y. Ang1,*, Thomas C. Brodnicki2,*, Margaret A. Jordan3, Wendy E. Wilson1, Pablo Silveira3,4, Briony L. Gliddon1, Alan G. Baxter3,{dagger} and Ian R. van Driel1,{dagger}

1 Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, VIC 3010, Australia
2 Molecular Medicine Division, The Walter and Eliza Hall Institute for Medical Research, Melbourne, VIC 3052, Australia
3 Comparative Genomics Centre, Molecular Sciences Building 21, James Cook University, Townsville QLD 4811, Australia
4 Present address: Garvan Institute of Medical Research, Autoimmunity Research Unit, Darlinghurst NSW 2010, Australia

Correspondence to: Ian R. van Driel; E-mail: i.vandriel{at}unimelb.edu.au

Autoimmune gastritis is a CD4+ T cell-mediated disease induced in genetically susceptible mice by thymectomy on the third day after birth. Previous linkage analysis indicated that Gasa1 and Gasa2, the major susceptibility loci for gastritis, are located on mouse chromosome 4. Here we verified these linkage data by showing that BALB.B6 congenic mice, in which the distal ~40 Mb of chromosome 4 was replaced by C57BL/6 DNA, were resistant to autoimmune gastritis. Analysis of further BALB.B6 congenic strains demonstrated that Gasa1 and Gasa2 can act independently to cause full expression of susceptibility to autoimmune disease. Gasa1 and Gasa2 are located between D4Mit352-D4Mit204 and D4Mit343-telomere, respectively. Numerical differences in Foxp3+ regulatory T cells were apparent between the BALB/c and congenic strains, but it is unlikely that this phenotype accounted for differences in autoimmune susceptibility. The positions of Gasa1 and Gasa2 correspond closely to the positions of Idd11 and Idd9, two autoimmune diabetes susceptibility loci in nonobese diabetic (NOD), mice and this prompted us to examine autoimmune gastritis in NOD mice. After neonatal thymectomy, NOD mice developed autoimmune gastritis, albeit at a slightly lower incidence and severity of disease than in BALB/c mice. Diabetes-resistant congenic NOD.B6 mice, harbouring a B6-derived interval encompassing the Gasa1/2-Idd9/11 loci, demonstrated a slight reduction in the incidence of autoimmune gastritis. This reduction was not significant compared with the reduction observed in BALB.B6 congenic mice, suggesting a difference in the genetic aetiology of autoimmune gastritis in NOD and BALB mice.

Keywords: autoimmune susceptibility genes, autoimmunity, T cells, tolerance

Transmitting editor: D. Tarlinton

*DKYA and TCB made similar contributions to this work.

{dagger} AGB and IRVD made similar contributions to this work.

Received 8 March 2007, accepted 26 June 2007.


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