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lüll HVEM/LIGHT/BTLA/CD160 cosignaling pathways as targets for immune regulation del Rio ML; Lucas CL; Buhler L; Rayat G; Rodriguez-Barbosa JIJ Leukoc Biol 2010[Feb]; 87 (2): 223-35Immunosuppression 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.|Animals[MESH]|Antigens, CD/*immunology[MESH]|Autoimmune Diseases/immunology/therapy[MESH]|GPI-Linked Proteins[MESH]|Graft Rejection/immunology/therapy[MESH]|Humans[MESH]|Receptors, Immunologic/*immunology[MESH]|Receptors, Tumor Necrosis Factor, Member 14/*immunology[MESH]|Signal Transduction/*immunology[MESH]|Tumor Necrosis Factor Ligand Superfamily Member 14/*immunology[MESH] |