Mayer L
Immunobiology Center, Box 1089, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029, USA.
Mt Sinai J Med. 2000 May;67(3):208-13.
An evolution in our understanding of the inflammatory bowel diseases (IBD), ulcerative colitis and Crohn's disease, correlates with increased knowledge of the function of the mucosal immune system. In the early 1960s and 1970s, IBD was considered to be an autoimmune disease in which there was a directed attack by humoral and cellular elements of the immune system against intestinal tissues. These studies did not withstand the test of time, and from the 1970s through the 1990s there was a growing appreciation that defects in cellular immunity, not auto-reactive in nature, played a larger role in disease pathogenesis. Research at Mount Sinai focused in on these cellular T cell defects and helped pave the way for the current model of disease pathogenesis.
我们对炎症性肠病（IBD）、溃疡性结肠炎和克罗恩病的理解演变，与对黏膜免疫系统功能的认识增加相关。在20世纪60年代初和70年代，IBD被认为是一种自身免疫性疾病，免疫系统的体液和细胞成分会直接攻击肠道组织。这些研究经不起时间的考验，从20世纪70年代到90年代，人们越来越认识到细胞免疫缺陷（本质上并非自身反应性）在疾病发病机制中起更大作用。西奈山的研究聚焦于这些细胞T细胞缺陷，并为当前的疾病发病机制模型奠定了基础。
