CD38 Controls the Innate Immune Response against Listeria monocytogenes
Open accessAbstract
CD38, adenosine-5′-diphosphate-ribosyl cyclase 1, is a multifunctional enzyme, expressed on a wide variety of cell types. CD38 has been assigned diverse functions, including generation of calcium-mobilizing metabolites, cell activation, and chemotaxis. Using a murine Listeria monocytogenes infection model, we found that CD38 knockout (KO) mice were highly susceptible to infection. Enhanced susceptibility was already evident within 3 days of infection, suggesting a function of CD38 in the innate immune response. CD38 was expressed on neutrophils and inflammatory monocytes, and especially inflammatory monocytes further upregulated CD38 during infection. Absence of CD38 caused alterations of the migration pattern of both cell types to sites of infection. We observed impaired accumulation of cells in the spleen but surprisingly similar or even higher accumulation of cells in the liver. CD38 KO and wild-type mice showed similar changes in the composition of neutrophils and inflammatory monocytes in blood and bone marrow, indicating that mobilization of these cells from the bone marrow was CD38 independent. In vitro , macrophages of CD38 KO mice were less efficient in uptake of listeria but still able to kill the bacteria. Dendritic cells also displayed enhanced CD38 expression following infection. However, absence of CD38 did not impair the capacity of mice to prime CD8 + T cells against L. monocytogenes , and CD38 KO mice could efficiently control secondary listeria infection. In conclusion, our results demonstrate an essential role for CD38 in the innate immune response against L. monocytogenes .
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CD38 regulates immune-cell homing, innate immune responses to pathogens and antitumour immunity.
“Previous studies have reported that CD38 regulates immune-cell homing, innate immune responses to pathogens and antitumour immunity63-65.”
From Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages (2020) · cites this paper as [64]
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Self-citation
- Authors
- Lischke, T., Heesch, K., Schumacher, V., Schneider, M., Haag, F., Koch-Nolte, F., & Mittrücker, H.-W.
- Affiliations
- University Medical Center Hamburg-Eppendorf (DE)
- Institute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 2013-11
- Volume
- 81
- Issue
- 11
- Pages
- 4091-4099
- ISSN
- 0019-9567 (ISSN-L)
- 1098-5522
- PMC
- PMC3811837
- OpenAlex
- W2117373786
- Cited by
- 92
- References
- 40
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 8 · 2023: 10 · 2022: 7 · 2021: 11 · 2020: 15 · 2019: 8 · 2018: 9 · 2017: 3 · 2016: 3 · 2015: 7 · 2014: 1
- FWCI
- 2.03
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Infection and Immunity (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Universitat de Barcelona
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- CD38, Listeria monocytogenes, innate immunity, neutrophils, inflammatory monocytes, dendritic cells, macrophages, cell migration, bacterial phagocytosis, CD8+ T cell priming, secondary infection, CD38 knockout mice
- MeSH terms
- Animals, Cell Movement, Dendritic Cells, Disease Models, Animal, Disease Susceptibility, Immunity, Innate, Listeriosis, Listeria monocytogenes, Liver, Macrophages, Membrane Glycoproteins, Monocytes, Neutrophils, Phagocytosis, Spleen, Gene Deletion, Mice, Knockout, Mice, ADP-ribosyl Cyclase 1, Host-Pathogen Interactions
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