Abstract
This review focuses on the biological functions and signalling pathways activated by Lymphotoxin α (LTα)/Lymphotoxin β (LTβ) and their receptor LTβR. Genetic mouse models shed light on crucial roles for LT/LTβR to build and to maintain the architecture of lymphoid organs and to ensure an adapted immune response against invading pathogens. However, chronic inflammation, autoimmunity, cell death or cancer development are disorders that occur when the LT/LTβR system is twisted. Biological inhibitors, such as antagonist antibodies or decoy receptors, have been developed and used in clinical trials for diseases associated to the LT/LTβR system. Recent progress in the understanding of cellular trafficking and NF-κB signalling pathways downstream of LTα/LTβ may bring new opportunities to develop therapeutics that target the pathological functions of these cytokines.
Copyright © 2011 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cell Death
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Gene Expression
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Humans
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Lymphotoxin alpha1, beta2 Heterotrimer / chemistry
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Lymphotoxin alpha1, beta2 Heterotrimer / immunology*
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Lymphotoxin beta Receptor / chemistry
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Lymphotoxin beta Receptor / immunology*
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Lymphotoxin-alpha / chemistry
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Lymphotoxin-alpha / genetics
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Lymphotoxin-alpha / immunology*
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Lymphotoxin-beta / chemistry
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Lymphotoxin-beta / genetics
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Lymphotoxin-beta / immunology*
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NF-kappa B / immunology
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Protein Structure, Tertiary
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Receptors, Tumor Necrosis Factor, Type I / chemistry
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Receptors, Tumor Necrosis Factor, Type I / immunology
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Receptors, Tumor Necrosis Factor, Type II / chemistry
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Receptors, Tumor Necrosis Factor, Type II / immunology
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Signal Transduction
Substances
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Lymphotoxin alpha1, beta2 Heterotrimer
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Lymphotoxin beta Receptor
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Lymphotoxin-alpha
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Lymphotoxin-beta
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NF-kappa B
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Receptors, Tumor Necrosis Factor, Type I
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Receptors, Tumor Necrosis Factor, Type II