Abstract
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.
MeSH terms
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Animals
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Autoimmune Diseases / immunology*
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Autoimmune Diseases / therapy*
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Cell Differentiation / drug effects
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Cell Differentiation / immunology
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Cell Movement / drug effects
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Cell Movement / immunology
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Chemokines / immunology
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Clinical Trials as Topic
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Humans
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Lymphocytes / drug effects
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Lymphocytes / immunology
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Lymphoid Tissue / drug effects
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Lymphoid Tissue / immunology
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Lymphotoxin alpha1, beta2 Heterotrimer / antagonists & inhibitors
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Lymphotoxin alpha1, beta2 Heterotrimer / immunology*
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Lymphotoxin beta Receptor / immunology*
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Models, Immunological
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Recombinant Fusion Proteins / administration & dosage
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Recombinant Fusion Proteins / immunology
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Signal Transduction / drug effects*
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Signal Transduction / immunology
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Stromal Cells / drug effects
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Stromal Cells / immunology
Substances
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Chemokines
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Lymphotoxin alpha1, beta2 Heterotrimer
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Lymphotoxin beta Receptor
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Recombinant Fusion Proteins