HVEM/LIGHT/BTLA/CD160 cosignaling pathways as targets for immune regulation

被引:130
作者
del Rio, M. L. [1 ]
Lucas, C. L. [2 ]
Buhler, L. [2 ,3 ]
Rayat, G. [4 ]
Rodriguez-Barbosa, J. I. [1 ]
机构
[1] Inst Biomed, Immunobiol Lab, Leon, Spain
[2] Harvard Univ, Massachusetts Gen Hosp, Bone Marrow Transplantat Sect,Sch Med, Transplantat Biol Res Ctr, Boston, MA USA
[3] Univ Hosp Geneva, Dept Surg, Surg Res Unit, Geneva, Switzerland
[4] Univ Alberta, Fac Med & Dent, Alberta Diabet Inst, Edmonton, AB, Canada
关键词
coinhibition; costimulation; transplantation; autoimmunity; T-LYMPHOCYTE ATTENUATOR; HERPESVIRUS ENTRY MEDIATOR; FACTOR RECEPTOR SUPERFAMILY; LYMPHOTOXIN-BETA RECEPTOR; MHC CLASS-I; B-LYMPHOCYTE; CELL-ACTIVATION; TNF SUPERFAMILY; FAMILY-MEMBER; NK CELLS;
D O I
10.1189/jlb.0809590
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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. J. Leukoc. Biol. 87: 223-235; 2010.
引用
收藏
页码:223 / 235
页数:13
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