作者: Marika C. Kullberg , Dragana Jankovic , Carl G. Feng , Sophie Hue , Peter L. Gorelick
DOI: 10.1084/JEM.20061082
关键词:
摘要: Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract that caused in part by dysregulated immune response to intestinal flora. The common interleukin (IL)-12/IL-23p40 subunit thought be critical for pathogenesis IBD. We have analyzed role IL-12 versus IL-23 two models Helicobacter hepaticus–triggered T cell–dependent colitis, one involving anti–IL-10R monoclonal antibody treatment infected cell–sufficient hosts, and other CD4+ cell transfer into Rag−/− recipients. Our data demonstrate not essential development maximal disease. Although has been implicated differentiation IL-17–producing cells alone are sufficient induce autoimmune tissue reactivity, our results instead support model which drives both interferon γ IL-17 responses together synergize trigger severe inflammation.