The Journal of Experimental Medicine
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Published online 13 December 2005 doi:10.1084/jem.20051984
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 12, 1643-1648
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BRIEF DEFINITIVE REPORT

 Hydronephrosis associated with antiurothelial and antinuclear autoantibodies in BALB/c-Fcgr2b–/–Pdcd1–/– mice

Taku Okazaki1,2, Yumi Otaka1, Jian Wang1,2, Hiroshi Hiai4, Toshiyuki Takai5, Jeffrey V. Ravetch6, and Tasuku Honjo3

1 Department of Medical Chemistry and Molecular Biology, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan
2 21st Century Center of Excellence Program, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan
3 Department of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan
4 Shiga Medical Center Research Institute, Shiga 524-8524, Japan
5 Department of Experimental Immunology and Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan
6 Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY 10021

CORRESPONDENCE Tasuku Honjo: honjo{at}mfour.med.kyoto-u.ac.jp

Because most autoimmune diseases are polygenic, analysis of the synergistic involvement of various immune regulators is essential for a complete understanding of the molecular pathology of these diseases. We report the regulation of autoimmune diseases by epistatic effects of two immunoinhibitory receptors, low affinity type IIb Fc receptor for IgG (Fc{gamma}RIIB) and programmed cell death 1 (PD-1). Approximately one third of the BALB/c-Fcgr2b–/–Pdcd1–/– mice developed autoimmune hydronephrosis, which is not observed in either BALB/c-Fcgr2b–/– or BALB/c-Pdcd1–/– mice. Hydronephrotic mice produced autoantibodies (autoAbs) against urothelial antigens, including uroplakin IIIa, and these antibodies were deposited on the urothelial cells of the urinary bladder. In addition, ~15% of the BALB/c-Fcgr2b–/–Pdcd1–/– mice produced antinuclear autoAbs. In contrast, the frequency of the autoimmune cardiomyopathy and the production of anti–parietal cell autoAb, which were observed in BALB/c-Pdcd1–/– mice, were not affected by the additional Fc{gamma}RIIB deficiency. These observations suggest cross talk between two immunoinhibitory receptors, Fc{gamma}RIIB and PD-1, on the regulation of autoimmune diseases.


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