Targeting T and B Lymphocytes in Inflammatory Bowel Diseases: Lessons from Clinical Trials

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
出处
期刊:Digestive Diseases [Karger Publishers]
卷期号:31 (3-4): 328-335 被引量:20
标识
DOI:10.1159/000354687
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-&#947; 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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