作者: Brian T. Wipke , Paul M. Allen
DOI: 10.4049/JIMMUNOL.167.3.1601
关键词: Ankle 、 Inflammation 、 Rheumatoid arthritis 、 Monoclonal antibody 、 Genetically modified mouse 、 Gene 、 Immunology 、 Medicine 、 Murine model 、 Serum transfer
摘要: Neutrophils are prominent participants in the joint inflammation of human rheumatoid arthritis (RA) patients, but extent their role inductive phase is unknown. In K/B×N mouse RA model, transfer autoreactive Ig from into mice induces a rapid and profound joint-specific inflammatory response reminiscent RA. We observed that after serum transfer, earliest clinical signs ankle correlated with presence neutrophils synovial regions recipient joints. this study, we investigated early to transferred arthritogenic transgenic mouse. Mice were treated neutrophil-depleting mAb before following scored for indications severity swelling joints front paws. absence neutrophils, completely resistant effects serum. Importantly, depletion diseased up 5 days reversed reaction Transfer deficient generation nitrogen or oxygen radicals ( inducible NO synthase 2 gp91 phox genes, respectively) gave normal responses, indicating neither pathway essential disease induction. These studies have identified critical initiating maintaining processes joint.