LIGHT/HVEM/LTβR interaction as a target for the modulation of the allogeneic immune response in transplantation.

M-L del Rio, P Schneider, C Fernandez-Renedo, J-A Perez-Simon, J-I Rodriguez-Barbosa

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 2013 Mar

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The exchange of information during interactions of T cells with dendritic cells, B cells or other T cells regulates the course of T, B and DC-cell activation and their differentiation into effector cells. The tumor necrosis factor superfamily member LIGHT (homologous to lymphotoxin, exhibits inducible expression and competes with HSV glycoprotein D for binding to herpesvirus entry mediator, a receptor expressed on T lymphocytes) is transiently expressed upon T cell activation and modulates CD8 T cell-mediated alloreactive responses upon herpes virus entry mediator (HVEM) and lymphotoxin β receptor (LTβR) engagement. LIGHT-deficient mice, or WT mice treated with LIGHT-targeting decoy receptors HVEM-Ig, LTβR-Ig or sDcR3-Ig, exhibit prolonged graft survival compared to untreated controls, suggesting that LIGHT modulates the course and severity of graft rejection. Therefore, targeting the interaction of LIGHT with HVEM and/or LTβR using recombinant soluble decoy receptors or monoclonal antibodies represent an innovative therapeutic strategy for the prevention and treatment of allograft rejection and for the promotion of donor-specific tolerance. © Copyright 2013 The American Society of Transplantation and the American Society of Transplant Surgeons.

Citation

M-L del Rio, P Schneider, C Fernandez-Renedo, J-A Perez-Simon, J-I Rodriguez-Barbosa. LIGHT/HVEM/LTβR interaction as a target for the modulation of the allogeneic immune response in transplantation. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons. 2013 Mar;13(3):541-51