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Contact-Free Co-Culture Model for the Study of Innate Immune Cell Activation During Respiratory Virus Infection
Published on: February 28, 2021
Co-stimulation: novel methods for preventing viral-induced lung inflammation
Tracy Hussell1, Robert Snelgrove, Ian R Humphreys
1Centre for Molecular Microbiology and Infection, Lord Flowers Building, Imperial College of Science, Technology and Medicine, Exhibition Road, London SW7 2AZ, UK. t.hussell@iperial.ac.uk
Abstract:
Respiratory infections cause significant morbidity and mortality worldwide. Although an immune response is required to eliminate respiratory pathogens, if unchecked, it can damage surrounding tissues and block primary lung function. Based on our knowledge of immune T-cell activation, there are several pathways to which immune intervention could be applied. However, relatively few interventions target only those immune cells that are responding to antigens. OX40 and 4-1BB are members of the tumour necrosis factor receptor family and are expressed on the surface of T cells in several inflammatory conditions. Recently, the inhibition of OX40 has proved beneficial during influenza virus infection. This review highlights the recent advances in the manipulation of such molecules and how they have been applied to inflammatory conditions that are caused by viruses in the lung.
Insights
Targeting immune cells like OX40 and 4-1BB offers new ways to treat lung inflammation from viral infections. Recent research shows inhibiting OX40 benefits influenza, suggesting potential for broader immune intervention in respiratory diseases.
Area of Science:
- Immunology
- Pulmonology
- Virology
Background:
- Respiratory infections lead to significant global morbidity and mortality.
- While the immune response is crucial for pathogen clearance, excessive inflammation can harm lung tissue and function.
- Existing immune interventions often lack specificity, targeting broadly rather than antigen-specific immune cells.
Purpose of the Study:
- To review recent advances in manipulating immune molecules like OX40 and 4-1BB.
- To explore the application of these manipulations in treating viral lung inflammatory conditions.
- To highlight the potential of targeted immune interventions for respiratory diseases.
Main Methods:
- Review of recent scientific literature on T-cell activation pathways.
- Analysis of studies investigating OX40 and 4-1BB receptor family members.
- Examination of therapeutic strategies involving immune cell modulation in viral infections.
Main Results:
- OX40 and 4-1BB are tumor necrosis factor receptor family members expressed on T cells during inflammation.
- Inhibition of OX40 has demonstrated efficacy in managing influenza virus infections.
- These findings suggest a potential for targeted immune intervention in viral lung diseases.
Conclusions:
- Targeting specific immune molecules offers a promising approach to managing inflammatory lung conditions.
- Modulation of OX40 and 4-1BB presents a potential therapeutic avenue for viral respiratory infections.
- Further research into targeted immune interventions could reduce morbidity and mortality associated with lung infections.
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