Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis

• DOI: 10.1084/jem.20020439
• Publication Date: 2002-07-28T22:32:53Z
• Authors: Hong Ji; Allison Pettit; Koichiro Ohmura; Adriana Ortiz-Lopez; Veronique Duchatelle; Claude Degott; Ellen Gravallese; Diane Mathis; Christophe Benoist
• Keywords: Inflammatory arthritis

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