A role for IL‐18 in protective immunity against Mycobacterium tuberculosis
Open accessAbstract
Tuberculosis remains the most hazardous bacterial infection worldwide. The causative agent, Mycobacterium tuberculosis, is a facultative intracellular pathogen of resting MΦ. IFN‐γ secreted by natural killer, CD4 Th 1 and CD8 T cells upon instruction by IL‐12 and ‐18 activates MΦ to restrict mycobacterial growth. Production of both cytokines is induced by TLR signalling in DC and MΦ. Mice deficient for the TLR adaptor, MyD88, are highly susceptible to M. tuberculosis infection. Shared usage of MyD88 by signalling cascades for TLR and receptors for IL‐1 and IL‐18 prompted us to revisit the role of IL‐18 during experimental infection with M. tuberculosis. We show that mice deficient for IL‐18 and MyD88 but not for IL‐18 receptor promptly succumbed to M. tuberculosis infection in contrast to WT or TLR‐2/‐4 double KO mice indicating that lack of IL‐18 contributes to the high susceptibility of MyD88 KO mice to M. tuberculosis. Without IL‐18, the protective Th1 response was decreased and hence, mycobacterial propagation was favoured. Neutrophil‐driven lung immunopathology concomitant with unrestrained growth of tubercle bacilli are most likely responsible for the premature death of IL‐18 KO mice. Thus, IL‐18 plays a decisive role in protective immunity against tuberculosis.
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Activated macrophages can limit growth of intracellular bacteria including M. tuberculosis and drive phagosome maturation toward phagolysosomes and auto-phagolysosomes.
“Activated MΦs can limit growth of intracellular bacteria including M. tuberculosis and drive phagosome maturation toward phagolysosomes and auto-phagolysosomes (54, 55).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [54]
IL-18 appears to be important to mount an efficient immune response because IL-18 knockout mice are more susceptible to M. tuberculosis infection than wildtype ones.
“Similarly to IL-1β, IL-18 appears to be of importance to mount an efficient immune response because IL-18 knockout mice are more susceptible to M. tuberculosis infection than wildtype ones.”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [54]
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- Authors
- Schneider, B. E., Korbel, D., Hagens, K., Koch, M., Raupach, B., Enders, J., Kaufmann, S. H. E., Mittrücker, H., & Schaible, U. E.
- Affiliations
- Max Planck Institute for Infection Biology (DE)
- London School of Hygiene & Tropical Medicine (GB)
- Corresponding author
- Schaible, Ulrich E.
- ORCID
- Venue
- European Journal of Immunology
- Publisher
- Wiley
- Published
- 2010-01-26
- Volume
- 40
- Issue
- 2
- Pages
- 396-405
- ISSN
- 0014-2980 (ISSN-L)
- 1521-4141
- PMC
- PMC3189623
- OpenAlex
- W1988950887
- Cited by
- 115
- References
- 47
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 3 · 2023: 10 · 2022: 1 · 2021: 10 · 2020: 3 · 2019: 5 · 2018: 6 · 2017: 9 · 2016: 8 · 2015: 3 · 2014: 11 · 2013: 10 · 2012: 10
- FWCI
- 6.44
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- European Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (submittedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- IL-18, Mycobacterium tuberculosis, tuberculosis, MyD88, IL-18 receptor, Th1 response, macrophages, neutrophils, lung immunopathology, protective immunity, Toll-like receptor signaling, interleukin-1, IL-12, interferon-gamma
- MeSH terms
- Analysis of Variance, Animals, Immunity, Interferon-gamma, Lung, Mice, Inbred C57BL, Mycobacterium tuberculosis, Tuberculosis, Gene Expression, Cytokines, Mice, Knockout, Th1 Cells, Chemokines, Genetic Predisposition to Disease, Reverse Transcriptase Polymerase Chain Reaction, Interleukin-18, Neutrophil Infiltration, Toll-Like Receptor 2, Toll-Like Receptor 4, Mice, Myeloid Differentiation Factor 88, Receptors, Interleukin-18
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