The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published 1 July 2002. doi:10.1084/jem.20020439
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© Rockefeller University Press, 0022-1007/2002/7/77/ $5.00
The Journal of Experimental Medicine, Volume 196, Number 1, July 1, 2002 77-85

Critical Roles for Interleukin 1 and Tumor Necrosis Factor {alpha} in Antibody-induced Arthritis

Hong Ji1,2, Allison Pettit3, Koichiro Ohmura1, Adriana Ortiz-Lopez1, Veronique Duchatelle4, Claude Degott4, Ellen Gravallese3, Diane Mathis1,2 and Christophe Benoist1,2

1 Section on Immunology and Immunogenetics, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215
2 Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé et de la Recherche Medicale/Université Louis Pasteur, 67404 Strasbourg, France
3 Beth Israel Deaconess Medical Center and New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, Boston, MA 02215
4 Service d'Anatomie et de Cytologie Pathologique, Hopital Beaujon, 92118 Clichy, France

Address correspondence to Diane Mathis and Christophe Benoist, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215. Phone: 617-264-2745; Fax: 617-264-2744; E-mail: cbdm{at}joslin.harvard.edu

In spontaneous inflammatory arthritis of K/BxN T cell receptor transgenic mice, the effector phase of the disease is provoked by binding of immunoglobulins (Igs) to joint surfaces. Inflammatory cytokines are known to be involved in human inflammatory arthritis, in particular rheumatoid arthritis, although, overall, the pathogenetic mechanisms of the human affliction remain unclear. To explore the analogy between the K/BxN model and human patients, we assessed the role and relative importance of inflammatory cytokines in K/BxN joint inflammation by transferring arthritogenic serum into a panel of genetically deficient recipients. Interleukin (IL)-1 proved absolutely necessary. Tumor necrosis factor (TNF)–{alpha} was also required, although seemingly less critically than IL-1, because a proportion of TNF-{alpha}–deficient mice developed robust disease. There was no evidence for an important role for IL-6. Bone destruction and reconstruction were also examined. We found that all mice with strong inflammation exhibited the bone erosion and reconstruction phenomena typical of K/BxN arthritis, with no evidence of any particular requirement for TNF{alpha} for bone destruction. The variability in the requirement for TNF-{alpha}, reminiscent of that observed in treated rheumatoid arthritis patients, did not appear genetically programmed but related instead to subtle environmental changes.

Key Words: transgenic • cytokine • knockout • inflammatory • TNF


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