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International Immunology, Vol. 12, No. 1, 1-8, January 2000
© 2000 Japanese Society for Immunology

Genetic regulation of anti-erythrocyte autoantibodies and splenomegaly in autoimmune hemolytic anemia-prone New Zealand Black mice

Kimiko Ochiai1, Shoichi Ozaki2, Akihiro Tanino1, Shinji Watanabe1, Tomoo Ueno1, Kenichi Mitsui3, Junichi Toei1, Yuji Inada1, Sachiko Hirose4, Toshikazu Shirai4 and Hiroyuki Nishimura1

1 Toin Human Science and Technology Center, Department of Biomedical Engineering, Toin University of Yokohama, 1614 Kurogane-cho, Aoba-ku, Yokohama 225-8502, Japan
2 Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan
3 Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, 4-1-8 Honmachi, Kawaguchi, Saitama 332-0012, Japan
4 Department of Pathology, Juntendo University School of Medicine, 2-1-1 Hongo Bunkyo-ku,Tokyo 113-8421, Japan

Correspondence to: H. Nishimura

New Zealand Black (NZB) mice spontaneously produce anti-erythrocyte autoantibodies (AEA) in association with splenomegaly, thus serving as a model for autoimmune hemolytic anemia. Although these autoimmune traits are inherited as a dominant fashion, expression in F1 hybrids of NZB and most non-New Zealand strains is suppressed due to the contribution of wild-type modifying genes present in the latter strains. Using chromosomal microsatellite markers in the (C57BL/6 x NZB)F1 x NZB backcross progeny, we mapped C57BL/6 modifying loci for AEA production and splenomegaly. Generation of AEA was found to be down-regulated by a combined effect of two major independently segregating dominant alleles—one linked to D7MIT30 on chromosome 7 and the other linked to D10MIT42 on chromosome 10. Splenomegaly was modified mainly by a single C57BL/6 allele linked to D4MIT58 on chromosome 4. Thus, the autoimmune hemolytic anemia in the NZB strain is under multigenic control and a combined action of not only susceptibility but also modifying alleles with suppressive activities affects the outcome of disease features in the progeny. There are potentially important candidate genes which may be linked to the regulation of AEA and splenomegaly.

Keywords: anti-erythrocyte autoantibody, hemolytic anemia, microsatellite, New Zealand Black mice, quantitative trait locus, splenomegaly

The first two authors contributed equally to this work

Transmitting editor: T. Saito


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