Sadlack B, Merz H, Schorle H, Schimpl A, Feller A C, Horak I
Institute of Virology and Immunobiology, University of Würzburg, Federal Republic of Germany.
Cell. 1993 Oct 22;75(2):253-61. doi: 10.1016/0092-8674(93)80067-o.
Mice deficient for interleukin-2 develop normally during the first 3-4 weeks of age. However, later on they become severely compromised, and about 50% of the animals die between 4 and 9 weeks after birth. Of the remaining mice, 100% develop an inflammatory bowel disease with striking clinical and histological similarity to ulcerative colitis in humans. The alterations of the immune system are characterized by a high number of activated T and B cells, elevated immunoglobulin secretion, anti-colon antibodies, and aberrant expression of class II major histocompatibility complex molecules. The data provide evidence for a primary role of the immune system in the etiology of ulcerative colitis and strongly suggest that the disease results from an abnormal immune response to a normal antigenic stimulus.
白细胞介素-2缺陷的小鼠在出生后的前3 - 4周发育正常。然而，之后它们的健康状况会严重受损，约50%的小鼠在出生后4至9周死亡。在存活下来的小鼠中，100%会患上炎症性肠病，其临床和组织学特征与人类溃疡性结肠炎极为相似。免疫系统的改变表现为大量活化的T细胞和B细胞、免疫球蛋白分泌增加、抗结肠抗体以及II类主要组织相容性复合体分子的异常表达。这些数据为免疫系统在溃疡性结肠炎病因学中的主要作用提供了证据，并有力地表明该疾病是由对正常抗原刺激的异常免疫反应所致。
