封锁
免疫学
疾病
医学
炎症性肠病
效应器
发病机制
抛物线性
病理
内科学
受体
作者
Takanori Kanai,Mamoru Watanabe,Toshifumi Hibi
出处
期刊:The Keio Journal of Medicine
[The Keio Journal of Medicine]
日期:2009-01-01
卷期号:58 (4): 203-209
被引量:4
摘要
Inflammatory bowel diseases (IBD) are thought to be caused by a complex interaction of genetic, immunological, and environmental factors. Why is it that once an IBD develops it lasts a long time? Considering this simple question, we propose that coliotogenic memory CD4+T cells that remember the prototype of the disease in each patient are formed in IBD at the onset, and, perceiving them as “benign T-cell leukemia”-like lifelong memory CD4+T cells that hematogenously spread throughout the body, we thus propose that systemic circulating colitogenic memory CD4+T cells would be an ideal target for the treatment of IBD. Accordingly, selective depletion of colitogenic memory CD4+T cells by leukocytapheresis and blockade of circulation of colitogenic memory CD4+T cells by a newly developed immunosuppressant, FTY720, may be associated with dramatic efficacy and a marked reduction of inflammatory cytokines produced by activated leucocytes. We here describe the immunological pathogenesis focusing on the generation of circulating colitogenic memory CD4+T cells and the possible logics of leukocytapheresis and FTY720 for the treatment of IBD.
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