Boismenu R, Chen Y
Department of Immunology and Strohm Inflammatory Bowel Disease Center, The Scripps Research Institute, La Jolla, California 92037, USA.
J Leukoc Biol. 2000 Mar;67(3):267-78. doi: 10.1002/jlb.67.3.267.
Emerging studies using mouse models of experimental colitis are defining the nature of the immunological disturbances that initiate inflammation and destruction of the intestine. A better understanding of disease-promoting and -suppressing CD4+ T cells is providing insight into the mechanisms controlling immune responses within the intestinal compartment. Moreover, a role for distinct T cell populations, including intraepithelial gammadelta T cells, in maintaining the physical integrity of the intestine was suggested by recent studies. Cytokine gene-knockout mice and anti-cytokine treatments remain important tools to define the pro- and anti-inflammatory functions of cytokines. These advances are fostering the design and evaluation of new therapeutic approaches that may eventually be applied to treat human inflammatory bowel disease.
利用实验性结肠炎小鼠模型开展的新研究正在明确引发肠道炎症和破坏的免疫紊乱的本质。对促进疾病和抑制疾病的CD4 + T细胞的更好理解,为深入了解肠道内免疫反应的控制机制提供了线索。此外,最近的研究表明,包括上皮内γδ T细胞在内的不同T细胞群体在维持肠道物理完整性方面发挥着作用。细胞因子基因敲除小鼠和抗细胞因子治疗仍然是确定细胞因子促炎和抗炎功能的重要工具。这些进展正在推动新治疗方法的设计和评估,这些方法最终可能应用于治疗人类炎症性肠病。