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International Immunology, Vol. 16, No. 3, pp. 455-465, March 2004
© 2004 Japanese Society for Immunology

FEATURED ARTICLE OF THE MONTH

The point mutation of tyrosine 759 of the IL-6 family cytokine receptor gp130 synergizes with HTLV-1 pX in promoting rheumatoid arthritis-like arthritis

Katsuhiko Ishihara1,3, Shin-ichiro Sawa3, Hideto Ikushima3, Seiichi Hirota4, Toru Atsumi2, Daisuke Kamimura3, Sung-Joo Park2, Masaaki Murakami3, Yukihiko Kitamura4, Yoichiro Iwakura5 and Toshio Hirano1,2,3

1 Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka, Japan 2 Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Kanagawa, Japan 3 Department of Molecular Oncology (C7), Osaka University Graduate School of Medicine, Suita, Osaka, Japan 4 Department of Pathology (C2), Osaka University Graduate School of Medicine, Suita, Osaka, Japan 5 Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo, Japan

Correspondence to: T. Hirano, Department of Molecular Oncology (C7), Osaka University Graduate School of Medicine, 2-2 Yamada-oka Suita, Osaka 565-0871, Japan. E-mail: hirano{at}molonc.med.osaka-u.ac.jp
Transmitting editor: H. Karasuyama

Rheumatoid arthritis (RA) is a polygenic autoimmune disease. The autoimmunity develops from synergistic actions of genetic and environmental factors. We generated a double-mutant mouse by crossing two murine models of RA, a gp130 mutant knock-in mouse (gp130F759/F759) and an HTLV-1 pX transgenic mouse (pX-Tg), in a C57BL/6 background, which is resistant to arthritis. The mice spontaneously developed severe arthritis with a much earlier onset than the gp130F759/F759 mice and with a much higher incidence than did the pX-Tg mice. The symptoms of gp130F759/F759 mice, including lymphoadenopathy, splenomegaly, hyper-{gamma}-globulinemia, autoantibody production, increases in memory/activated T cells and granulocytes in the peripheral lymphoid organs, and a decrease in the class II MHCbright CD11c+ population, were augmented in the double mutants. Marked reductions in incidence, severity and immunological abnormalities were seen in the triple mutant, IL-6–/–/gp130F759/F759/pX-Tg, indicating that the arthritis in the double mutant is IL-6 dependent. gp130F759/F759/pX-Tg is a unique mouse model for RA.

Keywords: autoimmune disease, knock-in mouse, rheumatoid arthritis, Tax


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