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Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
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Bacterial genotoxins induce T cell senescence
Sarah L Mathiasen1, Laura Gall-Mas1, Ioannis S Pateras2
1LEO Foundation Skin Immunology Research Center, Department of Immunology and Microbiology, University of Copenhagen, 2200 Copenhagen, Denmark.
Cell Reports
|June 9, 2021
Summary
Bacterial genotoxins, like cytolethal distending toxin (CDT), cause premature senescence in CD4 T cells, potentially disrupting adaptive immunity. This study links bacterial infections to T cell senescence via a specific signaling pathway.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Pathogenic bacteria produce genotoxins that damage host DNA.
- Genotoxins are implicated in immune response dysregulation, but mechanisms are unclear.
- T cells are critical for adaptive immunity.
Purpose of the Study:
- Investigate the effects of cytolethal distending toxin (CDT) on T cells.
- Elucidate the mechanisms by which bacterial genotoxins impact T cell function.
- Explore the link between bacterial infections and T cell senescence.
Main Methods:
- In vitro studies on activated CD4 T cells exposed to CDT.
- In vivo evidence of T cell senescence during genotoxin-producing bacterial infections.
- Analysis of the senescence-associated secretory phenotype (SASP) and ATM-p38 signaling.
Main Results:
- CDT induces premature senescence in activated CD4 T cells in vitro.
- Bacterial infection promotes T cell senescence in vivo.
- Senescent CD4 T cells exhibit a SASP orchestrated by the ATM-p38 signaling axis.
Conclusions:
- Bacterial genotoxins, particularly CDT, induce T cell senescence.
- This senescence involves a specific secretory phenotype (SASP) regulated by ATM-p38 signaling.
- Findings suggest a novel mechanism for bacterial immunomodulation and link infections to T cell aging.
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