Inhibition of the lymphotoxin pathway as a therapy for autoimmune disease.
The lymphotoxin (LT) system is part of the tumor necrosis factor family and is required for lymph node development. It has provided a wonderful tool for the dissection of processes critical not only for lymphoid organ development but also the maintenance of the adult immune architecture and the formation of ectopic organized lymphoid tissues in chronically inflamed sites. A soluble lymphotoxin-beta receptor-immunoglobulin (LTbetaR-Ig) fusion protein can block this pathway and is currently being tested in the treatment of autoimmune disease. This review focuses on the immunological consequences of combined LT and LIGHT inhibition with LTbetaR-Ig administration as distinct from the developmental biology.
Browning
Jeffrey L
JL
Department of Immunobiology, Biogen Idec, Cambridge, MA 02142, USA. jeff.browning@biogenidec.com
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology* / Q000628:therapy*; D002454:Cell Differentiation / Q000187:drug effects / Q000276:immunology; D002465:Cell Movement / Q000187:drug effects / Q000276:immunology; D018925:Chemokines / Q000276:immunology; D002986:Clinical Trials as Topic; D006801:Humans; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology; D008221:Lymphoid Tissue / Q000187:drug effects / Q000276:immunology; D053361:Lymphotoxin alpha1, beta2 Heterotrimer / Q000037:antagonists & inhibitors / Q000276:immunology*; D053259:Lymphotoxin beta Receptor / Q000276:immunology*; D018448:Models, Immunological; D011993:Recombinant Fusion Proteins / Q000008:administration & dosage / Q000276:immunology; D015398:Signal Transduction / Q000187:drug effects* / Q000276:immunology; D017154:Stromal Cells / Q000187:drug effects / Q000276:immunology
D018925:Chemokines; D053361:Lymphotoxin alpha1, beta2 Heterotrimer; D053259:Lymphotoxin beta Receptor; D011993:Recombinant Fusion Proteins