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Cited by 245Immune Cell Function and InteractionImmune Response and InflammationT-cell and B-cell Immunology

IL-1 β is required for IL-12 to induce production of IFN-γ by NK cells. A role for IL-1 β in the T cell-independent mechanism of resistance against intracellular pathogens

Hunter, C A, Chizzonite, R, Remington, J S·1995·The Journal of Immunology
DOI 10.4049/jimmunol.155.9.4347
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Abstract

Mice with the severe combined immunodeficiency (SCID) possess an IFN-gamma-dependent mechanism of resistance to the intracellular pathogens Toxoplasma gondii and Listeria monocytogenes that is dependent on IL-12-induced production of IFN-gamma by NK cells. In this report we demonstrate that IL-1 beta is required for IL-12 to stimulate production of IFN-gamma by NK cells, and that IL-1 is important in IL-12-mediated resistance to T. gondii in vivo. Stimulation of SCID mouse splenocytes with tachyzoites of T. gondii resulted in production of IFN-gamma. Addition of neutralizing Ab specific for IL-1 beta to these cultures inhibited completely the production of IFN-gamma. Similar results were obtained when LPS or L. monocytogenes were used to stimulate production of IFN-gamma by SCID mouse splenocytes. Addition of a neutralizing Ab to IL-1 alpha did not affect production of IFN-gamma by SCID mouse splenocytes stimulated with T. gondii, L. monocytogenes, or LPS. Stimulation of SCID mouse splenocytes with IL-1 beta or IL-1 alpha did not result in production of IFN-gamma but enhanced remarkably the ability of T. gondii or IL-12 to stimulate production of IFN-gamma. Furthermore, production of IFN-gamma by SCID mouse splenocytes stimulated with IL-12 plus TNF-alpha was completely ablated by anti-IL-1 beta, but not by anti-IL-1 alpha. Analysis of the culture supernatants of spleen cells from SCID mice stimulated with T. gondii or IL-12 plus TNF-alpha detected low levels of IL-1 beta; ad…

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  • TLR4 signaling is key in driving proinflammatory responses associated with COVID-19 and contributes to an increased Th1-type immune response because IL-18 (and IL-1β) strongly induces IFNs.

    “TLR4 signaling is key in driving proinflammatory responses associated with COVID-19 and contributes to an increased Th1-type immune response because IL-18 (and IL-1 β ) strongly induces IFNs. 143-145”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [143]

  • IL-18 strongly drives Th1 immune responses, but in BALB/c mice, this produces a mixed Th1/Th2 response that promotes fibrosis and DCM rather than a classical STAT-driven Th1 response.

    “IL-18, originally named IFNγ -inducing factor, strongly drives Th1 immune responses, 143-145 but in BALB/c mice, this produces a mixed Th1/Th2 response that promotes fibrosis and DCM rather than a classical STAT-driven Th1 respo nse. 115,146,160,165”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [143]

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Authors
Hunter, C. A., Chizzonite, R., & Remington, J. S.
Affiliations
Palo Alto Medical Foundation (US)
ORCID
Hunter, C A
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
1995-11-01
Volume
155
Issue
9
Pages
4347-4354
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.155.9.4347
OpenAlex
W2149673255
Cited by
245
References
0
Citations by year
2026: 1 · 2025: 1 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 12 · 2019: 6 · 2018: 3 · 2017: 6 · 2016: 6 · 2015: 6 · 2014: 10 · 2013: 9 · 2012: 8
FWCI
6.45
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Allergy and Infectious Diseases (AI 04717, AI30320)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
IL-1β, IL-12, interferon-gamma, natural killer cells, Toxoplasma gondii, Listeria monocytogenes, intracellular pathogens, T cell-independent immunity, IL-1 receptor, IL-1α, TNF-α, SCID mice, infection resistance, cytokine signaling, type I interferon, IL-18
MeSH terms
Adjuvants, Immunologic, Animals, Female, Immunity, Innate, Interferon-gamma, Interleukin-1, Killer Cells, Natural, Lipopolysaccharides, Listeria monocytogenes, Spleen, Toxoplasma, Toxoplasmosis, Animal, Mice, SCID, Interleukin-12, Mice

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