Laboratory of Immunobiology, Institute of Biomedicine, 24071-Leon, Spain.
J Leukoc Biol. 2010 Feb;87(2):223-35. doi: 10.1189/jlb.0809590. Epub 2009 Dec 9.
Immunosuppression is currently the treatment of choice to attenuate the chronic deterioration of tissue function as a result of the effector mechanisms of the immunological response in transplant rejection and autoimmune diseases. However, global immunosuppression greatly increases the risk of acquiring life-threatening infections and is associated with organ toxicity when used long-term. Thus, alternative approaches that inhibit only the unwanted immune responses and preserve general immunity are highly desirable. The receptor/ligand pairs involved in the cross-talk between DC and T cells have been the focus of intense and exciting research during the last decade. The HVEM/LIGHT/BTLA/CD160 costimulatory/coinhibitory pathway has emerged as a potential target for the development of immune therapeutic interventions. Herein, we will summarize and discuss how blockade of the costimulatory HVEM/LIGHT interaction or agonist signaling through the inhibitory BTLA and CD160 receptors could contribute to the control of deleterious immune responses.
免疫抑制是目前治疗选择，以减轻组织功能的慢性恶化，作为免疫反应的效应机制在移植排斥和自身免疫性疾病。然而，全身免疫抑制大大增加了获得危及生命的感染的风险，并与器官毒性长期使用时。因此，抑制仅不想要的免疫反应并保留一般免疫的替代方法是非常可取的。受体/配体对参与 DC 和 T 细胞之间的串扰一直是激烈和令人兴奋的研究的焦点在过去的十年。HVEM/LIGHT/BTLA/CD160 共刺激/共抑制途径已成为免疫治疗干预措施发展的一个潜在目标。在此，我们将总结和讨论如何阻断共刺激 HVEM/LIGHT 相互作用或通过抑制 BTLA 和 CD160 受体的激动剂信号，可能有助于控制有害的免疫反应。
