LIGHT–HVEM signaling and the regulation of T cell-mediated immunity
| Autor: | Sandra Rickert, Steve W. Granger |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Graft Rejection
Tumor Necrosis Factor Ligand Superfamily Member 14 Virus genetics T-Lymphocytes Endocrinology Diabetes and Metabolism T cell Immunology Gene Expression Graft vs Host Disease Biology Receptors Tumor Necrosis Factor General Biochemistry Genetics and Molecular Biology T cell mediated immunity Mice Immune system Neoplasms medicine Animals Humans Immunology and Allergy Cytotoxic T cell Mice Knockout Immunity Cellular Tumor Necrosis Factor-alpha Models Immunological Membrane Proteins Dendritic Cells Cell biology TNF receptor associated factor medicine.anatomical_structure Receptors Virus Decoy receptor 3 Lymphotoxin beta receptor Receptors Tumor Necrosis Factor Member 14 Signal Transduction |
| Zdroj: | Cytokine & Growth Factor Reviews. 14:289-296 |
| ISSN: | 1359-6101 |
| Popis: | LIGHT is a tumor necrosis factor (TNF) superfamily ligand that regulates T cell immune responses by signaling through the herpes virus entry mediator (HVEM) and the lymphotoxin beta receptor (LTbetaR). This review will present a summary of recent advances made regarding the immunobiology of the LIGHT-HVEM and LTbetaR systems. LIGHT has emerged as a potent initiator of T cell co-stimulation signals effecting CTL-mediated tumor rejection, allograft rejection and graft versus host disease. Constitutive expression of LIGHT leads to tissue destruction and autoimmune-like disease syndromes. In contrast to LTalphabeta, LIGHT plays a minimal role in lymphoid tissue development, yet some evidence indicates a role in negative selection in the thymus. These results provide an encouraging profile for the LIGHT-HVEM-LTbetaR axis as a potential target for controlling cellular immune reactions. |
| Databáze: | OpenAIRE |
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