Goetz Martin, Atreya Raja, Ghalibafian Maryam, Galle Peter R, Neurath Markus F
I. Medical Clinic, University of Mainz, Germany.
Inflamm Bowel Dis. 2007 Nov;13(11):1365-8. doi: 10.1002/ibd.20215.
B-cells are considered to play a pathogenic role in human ulcerative colitis (UC) by producing autoantibodies that cause epithelial cell damage. Here we report on a patient with intractable UC who suffered from a severe exacerbation of UC after salvage therapy with rituximab, a B-cell-depleting anti-CD20-antibody.
A 58-year-old patient with active long-standing UC and unresponsiveness or adverse events to mesalamine, corticosteroids, azathioprine, methotrexate, infliximab, leukapheresis, mycophenolate mofetil, and adalimumab received 375 mg/m(2) rituximab.
A severe exacerbation of UC activity was noted upon therapy that required hospitalization. Subsequent studies showed a complete depletion of CD20-positive mucosal B-cells associated with a suppression of local IL-10 production.
In contrast to rheumatoid arthritis patients, rituximab had deleterious effects in our UC patient by blocking IL-10 producing B-cells. Our data suggest an important anti- rather than proinflammatory role of B-cells in UC.
B细胞被认为通过产生导致上皮细胞损伤的自身抗体在人类溃疡性结肠炎（UC）中发挥致病作用。在此，我们报告一名难治性UC患者，在用利妥昔单抗（一种耗竭B细胞的抗CD20抗体）进行挽救治疗后，UC病情严重恶化。
一名58岁的长期活动性UC患者，对美沙拉嗪、皮质类固醇、硫唑嘌呤、甲氨蝶呤、英夫利昔单抗、白细胞去除术、霉酚酸酯和阿达木单抗无反应或出现不良事件，接受了375 mg/m²的利妥昔单抗治疗。
治疗期间观察到UC活动严重恶化，需要住院治疗。随后的研究表明，CD20阳性黏膜B细胞完全耗竭，同时局部IL-10产生受到抑制。
与类风湿关节炎患者不同，利妥昔单抗通过阻断产生IL-10的B细胞，对我们的UC患者产生了有害影响。我们的数据表明，B细胞在UC中起重要的抗炎而非促炎作用。
