Macrophage Interplay with Pore-Forming Toxins
A special issue of Toxins (ISSN 2072-6651).
Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 15739
Special Issue Editor
Interests: pore-forming toxins; cholesterol-dependent cytolysins; membrane repair; DNases; lupus
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
One critical innate immune cell type is the macrophage. Macrophages play key roles in pathogen clearance and tissue repair. Many pathogens secrete pore-forming toxins (PFTs), which macrophages must detect, then defend against them and respond to them. Similarly, macrophages also detect and respond to innate immune PFTs deployed against bacteria, and target cells, including perforin and the membrane, attack the complex of complement. Finally, macrophages themselves utilize PFTs like gasdermin D and mixed-lineage kinase-like (mlkl) to execute the cell death pathways of pyroptosis and necroptosis, respectively, to deny intracellular pathogens refuge. Interplay between macrophages and toxins occurs at many steps and leaves many unknowns in the field. Three broad outstanding questions in the field are: How do macrophages discriminate between PFTs to correctly promote or suppress inflammation? What molecular mechanisms drive macrophage responses to PFTs? How do bacteria and other pathogens hijack macrophage responses to PFTs to promote infection?
This Special Issue will focus on the interplay between macrophages and related myeloid cells with pore-forming toxins, including both the use of pore-forming toxins by these cells, and the response of these cells to toxins. This includes the biology behind cell death processes that require pore-forming toxins, macrophage responses to external toxins deployed against other bacteria and cells, and inflammation, immunosuppression, signaling, and other responses to pore-forming toxins.
Asst. Prof. Dr. Peter A. Keyel
Guest Editor
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Keywords
- pore-forming toxin
- pyroptosis
- mlkl
- inflammation
- host–pathogen interaction
- cell death
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