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Network communications: lymphotoxins, LIGHT, and TNF.
1Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, California 92121, USA. cware@liai.org
Annual Review of Immunology
|March 18, 2005
Summary
Lymphotoxins (LT), tumor necrosis factor (TNF), and LIGHT form a crucial immune signaling network. Disrupting this network can treat autoimmune diseases but may reduce pathogen resistance, revealing complex roles in immunity and disease.
Area of Science:
- Immunology
- Molecular Biology
- Cell Signaling
Background:
- Lymphotoxins (LT), tumor necrosis factor (TNF), and LIGHT (LT-related inducible ligand) form an integrated signaling network.
- This network is vital for innate and adaptive immune responses, regulating lymphoid tissue microenvironments and host defense.
- Signaling pathways involving chemokines and interferons are regulated by this network.
Purpose of the Study:
- To investigate the role of the LT/TNF/LIGHT signaling network in immune responses and autoimmune diseases.
- To understand the consequences of disrupting this network in preclinical models and human conditions.
Main Methods:
- Review of recent studies on lymphotoxin signaling pathways.
- Analysis of data from autoimmune disease models and clinical trials in rheumatoid arthritis.
Main Results:
- Disruption of the LT/TNF/LIGHT network reduced inflammation in some autoimmune models but impaired host defense against certain pathogens.
- Pharmacological disruption alleviated inflammation in a subset of rheumatoid arthritis patients, indicating varied responses.
Conclusions:
- The LT/TNF/LIGHT network plays a complex role in both autoimmunity and host defense.
- Varied responses to network disruption challenge current understanding of autoimmunity and suggest novel pathogenic roles.