CD137-CD137 Ligand Interactions in Inflammation.
CD137-CD137 Ligand Interactions in Inflammation.
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DOI：
10.4110/in.2009.9.3.84
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发表时间：
2009-06
期刊：
影响因子：
6
通讯作者：
Kwon B
中科院分区：
文献类型：
--
作者：
Kwon B
CD137研究的主流是针对CD137在CD8+ t细胞免疫中的功能，包括其抗肿瘤活性，以及与之矛盾的CD137的免疫抑制活性，这证明了CD137在多种自身免疫性和炎症性疾病的动物模型中具有很大的治疗潜力。然而，最近的研究为CD137的生物学添加了复合物。越来越多的证据支持CD137受体及其配体（CD137L）存在双向信号转导途径。CD137/CD137L相互作用参与造血细胞和非造血细胞的网络，除了抗原呈递细胞- t细胞相互作用。通过CD137L发出的信号在髓细胞的分化及其细胞活动中起着关键作用，表明CD137L信号触发并维持炎症。综上所述，CD137L引起的炎症放大可能通过上调共刺激分子、MHC分子、细胞粘附分子、细胞因子和趋化因子，增强t细胞活性和CD137信号。解决这一突出问题迫在眉睫，并将具有重要的临床意义。
The main stream of CD137 studies has been directed to the function of CD137 in CD8+ T-cell immunity, including its anti-tumor activity, and paradoxically the immunosuppressive activity of CD137, which proves to be of a great therapeutic potential for animal models of a variety of autoimmune and inflammatory diseases. Recent studies, however, add complexes to the biology of CD137. Accumulating is evidence supporting that there exists a bidirectional signal transduction pathway for the CD137 receptor and its ligand (CD137L). CD137/CD137L interactions are involved in the network of hematopoietic and nonhematopoietic cells in addition to the well characterized antigen-presenting cell-T cell interactions. Signaling through CD137L plays a critical role in the differentiation of myeloid cells and their cellular activities, suggesting that CD137L signals trigger and sustain inflammation. The overall consequence might be that the amplified inflammation by CD137L enhances the T-cell activity together with CD137 signals by upregulating costimulatory molecules, MHC molecules, cell adhesion molecules, cytokines, and chemokines. Solving this outstanding issue is urgent and will have an important clinical implication.