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 Blood, 15 August 2005, Vol. 106, No. 4, pp. 1323-1329.
Prepublished online as a Blood First Edition Paper on April 28, 2005; DOI 10.1182/blood-2005-02-0558.

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Submitted February 9, 2005
Accepted April 14, 2005

Identification of two major loci linked to autoimmune hemolytic anemia in NZB mice

Shuichi Kikuchi, Hirofumi Amano, Eri Amano, Liliane Fossati-Jimack, Marie-Laure Santiago-Raber, Thomas Moll, Akinori Ida, Brian L Kotzin, and Shozo Izui*

Department of Pathology and Immunology, Centre Medical Universitaire, Geneva, Switzerland
Rheumatology Section, Hammersmith Campus, Imperial College School of Medicine, London, United Kingdom
Division of Clinical Immunology, University of Colorado Health Sciences Center and National Jewish Medical and Research Center, Denver, Colorado, USA

* Corresponding author; email: Shozo.Izui{at}medecine.unige.ch.

Using a cohort of C57BL/6 (B6) x (NZB x B6)F1 backcross male mice bearing the Yaa (Y-linked autoimmune acceleration) mutation, we mapped and characterized the NZB-derived susceptibility loci predisposing to the development of autoimmune hemolytic anemia (AHA). Our analysis identified two major loci on NZB chromosome 7 and chromosome 1 linked with Coombs' anti-erythrocyte autoantibody production, and their contributions were confirmed by the analysis of B6.Yaa mice congenic for each NZB-derived susceptibility interval. A newly identified Aia3 (autoimmune anemia 3) locus present on NZB chromosome 7 selectively regulated Coombs antibody responses, while the second locus, directly overlapping with Nba2 (NZB autoimmunity 2) on chromosome 1, promoted the development of AHA, likely as part of its effect on overall production of lupus autoantibodies. A higher incidence of Coombs' antibody production in B6.Aia3 congenic mice than B6.Nba2 mice indicated a major role for Aia3 in AHA. Notably, lack of expansion of B1 cells in B6.Aia3 congenic mice argued against the involvement of this subset in AHA. Finally, our analysis of BC mice also demonstrated the presence of a B6-derived H2-linked locus on chromosome 17 that apparently regulated the production of Coombs' antibodies as a result of its overall autoimmune promoting effect.


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