Bouma Gerd, Strober Warren
The Mucosal Immunity Section, National Institutes of Health, Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institutes of Allergy and Infectious Diseases, 10 Center Drive, Room 11N238, Bethesda, Maryland 20892, USA.
Nat Rev Immunol. 2003 Jul;3(7):521-33. doi: 10.1038/nri1132.
The inflammatory bowel diseases (IBDs), Crohn's disease and ulcerative colitis, are chronic inflammatory disorders of the gastrointestinal tract. Enormous progress has been made recently in understanding the pathogenesis of these diseases. Through the study of patients and mouse models, it has emerged that Crohn's disease is driven by the production of interleukin-12 (IL-12) and interferon-gamma (IFN-gamma), whereas ulcerative colitis is probably driven by the production of IL-13. A second area of progress is in the identification of specific genetic abnormalities that are responsible for disease. The most important finding is the identification of mutations in the gene that encodes NOD2 (nucleotide-binding oligomerization domain 2) protein in a subgroup of patients with Crohn's disease. Here, we discuss these recent findings and the implications for therapy.
炎症性肠病(IBD),即克罗恩病和溃疡性结肠炎,是胃肠道的慢性炎症性疾病。最近在了解这些疾病的发病机制方面取得了巨大进展。通过对患者和小鼠模型的研究发现,克罗恩病是由白细胞介素-12(IL-12)和干扰素-γ(IFN-γ)的产生所驱动,而溃疡性结肠炎可能是由IL-13的产生所驱动。进展的第二个领域是确定导致疾病的特定基因异常。最重要的发现是在一部分克罗恩病患者中鉴定出编码NOD2(核苷酸结合寡聚化结构域2)蛋白的基因突变。在此,我们讨论这些最新发现及其对治疗的意义。