Autoimmune diseases, like rheumatoid arthritis, result from a dysregulation of the immune response culminating in hyperactivation of effector cells leading to immune-mediated injury. To maintain an appropriate immune response and prevent the emergence of autoimmune disease, activation signals must be regulated by inhibitory pathways. Biochemical and genetic studies indicate that the type IIB low-affinity receptor for immunoglobulin (Ig)G (FcγRIIB) inhibits cellular activation triggered through antibody or immune complexes and may be an important component in preventing the emergence of autoimmunity. To investigate the role of FcγRIIB in the development of type II collagen (CII)-induced arthritis (CIA), a model for rheumatoid arthritis in humans, we have examined its contribution in determining the susceptibility to CIA in the nonpermissive H-2b haplotype. H-2b mice immunized with bovine CII do not develop appreciable disease. In contrast, immunization of the FcγRIIB-deficient, H-2b mice with bovine CII induced CIA at an incidence of 42.2%. The maximal arthritis index of the FcγRIIB-deficient mice developing CIA (6.9 ± 3.6) was comparable to that of DBA/1 mice (8.6 ± 1.9), an H-2q strain susceptible for CIA induction. IgG1, IgG2a, and IgG2b antibody responses against CII were elevated in the FcγRIIB-deficient animals, especially in those mice showing arthritis, but less pronounced than DBA/1 mice. Histological examinations of the arthritic paws from FcγRIIB-deficient mice revealed that cartilage was destroyed and bone was focally eroded in association with marked lymphocyte and monocyte/macrophage infiltration, very similar to the pathologic findings observed in DBA/1 mice. These results indicate that a nonpermissive H-2b haplotype can be rendered permissive to CIA induction through deletion of FcγRIIB, suggesting that FcγRIIB plays a critical role in suppressing the induction of CIA.
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4 January 1999
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January 04 1999
Deletion of Fcγ Receptor IIB Renders H-2b Mice Susceptible to Collagen-induced Arthritis
Takae Yuasa,
Takae Yuasa
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
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Satoshi Kubo,
Satoshi Kubo
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
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Tadashi Yoshino,
Tadashi Yoshino
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
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Azusa Ujike,
Azusa Ujike
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
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Kimio Matsumura,
Kimio Matsumura
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
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Masao Ono,
Masao Ono
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
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Jeffrey V. Ravetch,
Jeffrey V. Ravetch
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
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Toshiyuki Takai
Toshiyuki Takai
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
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Takae Yuasa
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
Satoshi Kubo
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
Tadashi Yoshino
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
Azusa Ujike
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
Kimio Matsumura
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
Masao Ono
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
Jeffrey V. Ravetch
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
Toshiyuki Takai
From the *Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ‡Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Tokyo 101-0062, Japan; the §Second Department of Pathology, Okayama University Medical School, Okayama 700-8558, Japan; and the ‖Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York 10021
Address correspondence to Toshiyuki Takai, Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo, Sendai 980-8575, Japan. Phone: 81-22-717-8501; Fax: 81-22-717-8505; E-mail: [email protected]
Received:
October 08 1998
Revision Received:
October 26 1998
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1999
J Exp Med (1999) 189 (1): 187–194.
Article history
Received:
October 08 1998
Revision Received:
October 26 1998
Citation
Takae Yuasa, Satoshi Kubo, Tadashi Yoshino, Azusa Ujike, Kimio Matsumura, Masao Ono, Jeffrey V. Ravetch, Toshiyuki Takai; Deletion of Fcγ Receptor IIB Renders H-2b Mice Susceptible to Collagen-induced Arthritis . J Exp Med 4 January 1999; 189 (1): 187–194. doi: https://doi.org/10.1084/jem.189.1.187
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