Mpeg1 is not essential for antibacterial or antiviral immunity, but is implicated in antigen presentation.
Ebrahimnezhaddarzi, S
Bird, CH
Allison, CC
Tuipulotu, DE
Kostoulias, X
Macri, C
Stutz, MD
Abraham, G
Kaiserman, D
Pang, SS
Man, SM
Mintern, JD
Naderer, T
Peleg, AY
Pellegrini, M
Whisstock, JC
Bird, PI
- Publisher:
- WILEY
- Publication Type:
- Journal Article
- Citation:
- Immunol Cell Biol, 2022, 100, (7), pp. 529-546
- Issue Date:
- 2022-08
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Ebrahimnezhaddarzi, S | |
dc.contributor.author | Bird, CH | |
dc.contributor.author | Allison, CC | |
dc.contributor.author | Tuipulotu, DE | |
dc.contributor.author | Kostoulias, X | |
dc.contributor.author | Macri, C | |
dc.contributor.author | Stutz, MD | |
dc.contributor.author | Abraham, G | |
dc.contributor.author | Kaiserman, D | |
dc.contributor.author | Pang, SS | |
dc.contributor.author | Man, SM | |
dc.contributor.author | Mintern, JD | |
dc.contributor.author | Naderer, T | |
dc.contributor.author | Peleg, AY | |
dc.contributor.author | Pellegrini, M | |
dc.contributor.author | Whisstock, JC | |
dc.contributor.author | Bird, PI | |
dc.date.accessioned | 2025-01-15T13:30:28Z | |
dc.date.available | 2022-04-25 | |
dc.date.available | 2025-01-15T13:30:28Z | |
dc.date.issued | 2022-08 | |
dc.identifier.citation | Immunol Cell Biol, 2022, 100, (7), pp. 529-546 | |
dc.identifier.issn | 0818-9641 | |
dc.identifier.issn | 1440-1711 | |
dc.identifier.uri | http://hdl.handle.net/10453/183652 | |
dc.description.abstract | To control infections phagocytes can directly kill invading microbes. Macrophage-expressed gene 1 (Mpeg1), a pore-forming protein sometimes known as perforin-2, is reported to be essential for bacterial killing following phagocytosis. Mice homozygous for the mutant allele Mpeg1tm1Pod succumb to bacterial infection and exhibit deficiencies in bacterial killing in vitro. Here we describe a new Mpeg mutant allele Mpeg1tm1.1Pib on the C57BL/6J background. Mice homozygous for the new allele are not abnormally susceptible to bacterial or viral infection, and irrespective of genetic background show no perturbation in bacterial killing in vitro. Potential reasons for these conflicting findings are discussed. In further work, we show that cytokine responses to inflammatory mediators, as well as antibody generation, are also normal in Mpeg1tm1.1Pib/tm1.1Pib mice. We also show that Mpeg1 is localized to a CD68-positive endolysosomal compartment, and that it exists predominantly as a processed, two-chain disulfide-linked molecule. It is abundant in conventional dendritic cells 1, and mice lacking Mpeg1 do not present the model antigen ovalbumin efficiently. We conclude that Mpeg1 is not essential for innate antibacterial protection or antiviral immunity, but may play a focused role early in the adaptive immune response. | |
dc.format | Print-Electronic | |
dc.language | eng | |
dc.publisher | WILEY | |
dc.relation.ispartof | Immunol Cell Biol | |
dc.relation.isbasedon | 10.1111/imcb.12554 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | 0601 Biochemistry and Cell Biology, 1107 Immunology | |
dc.subject.classification | Immunology | |
dc.subject.classification | 3101 Biochemistry and cell biology | |
dc.subject.classification | 3204 Immunology | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Antigen Presentation | |
dc.subject.mesh | Bacterial Infections | |
dc.subject.mesh | Immunity, Innate | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Pore Forming Cytotoxic Proteins | |
dc.subject.mesh | Virus Diseases | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Bacterial Infections | |
dc.subject.mesh | Virus Diseases | |
dc.subject.mesh | Antigen Presentation | |
dc.subject.mesh | Pore Forming Cytotoxic Proteins | |
dc.subject.mesh | Immunity, Innate | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Antigen Presentation | |
dc.subject.mesh | Bacterial Infections | |
dc.subject.mesh | Immunity, Innate | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Pore Forming Cytotoxic Proteins | |
dc.subject.mesh | Virus Diseases | |
dc.title | Mpeg1 is not essential for antibacterial or antiviral immunity, but is implicated in antigen presentation. | |
dc.type | Journal Article | |
utslib.citation.volume | 100 | |
utslib.location.activity | United States | |
utslib.for | 0601 Biochemistry and Cell Biology | |
utslib.for | 1107 Immunology | |
pubs.organisational-group | University of Technology Sydney | |
pubs.organisational-group | University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | open_access | * |
dc.rights.license | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by-nc-nd/4.0/ | |
dc.date.updated | 2025-01-15T13:30:25Z | |
pubs.issue | 7 | |
pubs.publication-status | Published | |
pubs.volume | 100 | |
utslib.citation.issue | 7 |
Abstract:
To control infections phagocytes can directly kill invading microbes. Macrophage-expressed gene 1 (Mpeg1), a pore-forming protein sometimes known as perforin-2, is reported to be essential for bacterial killing following phagocytosis. Mice homozygous for the mutant allele Mpeg1tm1Pod succumb to bacterial infection and exhibit deficiencies in bacterial killing in vitro. Here we describe a new Mpeg mutant allele Mpeg1tm1.1Pib on the C57BL/6J background. Mice homozygous for the new allele are not abnormally susceptible to bacterial or viral infection, and irrespective of genetic background show no perturbation in bacterial killing in vitro. Potential reasons for these conflicting findings are discussed. In further work, we show that cytokine responses to inflammatory mediators, as well as antibody generation, are also normal in Mpeg1tm1.1Pib/tm1.1Pib mice. We also show that Mpeg1 is localized to a CD68-positive endolysosomal compartment, and that it exists predominantly as a processed, two-chain disulfide-linked molecule. It is abundant in conventional dendritic cells 1, and mice lacking Mpeg1 do not present the model antigen ovalbumin efficiently. We conclude that Mpeg1 is not essential for innate antibacterial protection or antiviral immunity, but may play a focused role early in the adaptive immune response.
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