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Updated: Aug 5, 2026
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Following in Real Time the Impact of Pneumococcal Virulence Factors in an Acute Mouse Pneumonia Model Using Bioluminescent Bacteria
Published on: February 23, 2014
Pneumococcal transmission is driven by TNFR2+ regulatory T-cells
Daan Beentjes1, James Murray1, Neil French1
1Department of Clinical Infection, Microbiology and Immunology, University of Liverpool, Liverpool, United Kingdom.
Frontiers in Immunology
|August 4, 2026
Summary
Regulatory T-cells expressing TNF receptor-2 (TNFR2+ Tregs) surprisingly promote the transmission of hypervirulent pneumococcal strains. This immune suppression enhances bacterial carriage and spread, highlighting a new target for vaccines and therapies.
Area of Science:
- Immunology
- Microbiology
- Epidemiology
Background:
- * Pneumococcal serotype 1, sequence type 217 (ST217), drives invasive disease outbreaks in Sub-Saharan Africa, causing substantial illness and death.
- * Understanding ST217 transmission is crucial for effective vaccine and therapeutic strategies.
Purpose of the Study:
- * To investigate the transmission dynamics of the hypervirulent pneumococcal strain ST217.
- * To elucidate the host immune mechanisms influencing ST217 transmission in a relevant model.
Main Methods:
- * Utilized an adolescent mouse model to study pneumococcal transmission dynamics.
- * Analyzed the role of regulatory T-cells (Tregs) and their interaction with other immune cells during colonization.
Main Results:
- * Found that TNFR2-positive Tregs suppress IL-17A-producing γδT and Th17 cells, impairing neutrophil-mediated clearance of ST217.
- * Demonstrated that this immune suppression increases ST217 carriage density and nasal shedding, facilitating transmission.
- * Showed that pneumolysin toxin drives TNFR2+ Treg responses in a strain-dependent manner, contrasting with low-transmission strains like serotype 23F.
Conclusions:
- * Demonstrated an unexpected, critical role for TNFR2+ Tregs in promoting the transmission of hypervirulent pneumococci.
- * Identified a novel mechanism involving immune suppression that enhances pneumococcal spread, offering potential targets for intervention.
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