医学
免疫学
炎症性肠病
T细胞
溃疡性结肠炎
炎症
美罗华
抗体
免疫系统
疾病
内科学
作者
Romana R. Gerner,Alexander R. Moschen,Herbert Tilg
摘要
Both innate and adaptive immunity play an important role in the pathogenesis of inflammatory bowel diseases (IBDs). There is strong evidence that especially activated T cells initiate and perpetuate inflammation and tissue destruction. The increased numbers of CD4<sup>+</sup> T cells in the intestinal wall of IBD patients may be explained by enhanced influx/activation and decreased apoptosis of these cells. Several studies have demonstrated that the gut-homing receptors CCR9 and α4β7 are selectively induced on T cells during their priming in intestinal inflamed sites. Whereas targeting of activated CD4<sup>+</sup> T cells by specific antibody strategies or neutralization of key T-cell cytokines such as IL-2 or IFN-γ has not been effective in human IBD, blocking migration of activated leukocytes, e.g. T cells into the inflamed tissue by specific antibodies such as vedolizumab, seems highly effective. Recently it could also been demonstrated that administration of antigen-specific regulatory T cells to patients with refractory Crohn's disease was not only well tolerated but showed promising results. The role of B cells in human IBD is less clear. B-cell depletion has so far only been studied in ulcerative colitis where rituximab (anti-CD20) therapy failed. Therefore, although the therapeutic targeting of ‘inflammatory' T and B cells was not successful in IBD, especially T cells remain key players in IBD. Targeting either T-cell migration or the use of regulatory T cells appears as the most promising ‘T-cell-directed' therapies in the future.
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