Cited by 418Tuberculosis Research and EpidemiologyImmune Response and Inflammationinterferon and immune responses

Innate and Adaptive Interferons Suppress IL-1α and IL-1β Production by Distinct Pulmonary Myeloid Subsets during Mycobacterium tuberculosis Infection

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Mayer-Barber, Katrin D., Andrade, Bruno B., Barber, Daniel L., Hieny, Sara, Feng, Carl G., Caspar, Patricia, Oland, Sandy, Gordon, Siamon +1 more·2011·Immunity

Abstract

Interleukin-1 (IL-1) receptor signaling is necessary for control of Mycobacterium tuberculosis (Mtb) infection, yet the role of its two ligands, IL-1α and IL-1β, and their regulation in vivo are poorly understood. Here, we showed that both IL-1α and IL-1β are critically required for host resistance and identified two multifunctional inflammatory monocyte-macrophage and DC populations that coexpressed both IL-1 species at the single-cell level in lungs of Mtb-infected mice. Moreover, we demonstrated that interferons (IFNs) played important roles in regulating IL-1 production by these cells in vivo. Type I interferons inhibited IL-1 production by both subsets whereas CD4(+) T cell-derived IFN-γ selectively suppressed monocyte-macrophages. These data provide a cellular basis for both the anti-inflammatory effects of IFNs and probacterial functions of type I IFNs during Mtb infection and reveal differential regulation of IL-1 production by distinct cell populations as an additional layer of complexity in the activity of IL-1 in vivo.

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Crossref · 10.1016/j.immuni.2011.12.002

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  • IL-1β is massively induced upon infection of macrophages with M. tuberculosis and plays important roles in anti-mycobacterial immune defenses because knockout mice are more susceptible to this infection.

    “IL-1β is massively induced upon infection of macrophages with M. tuberculosis, and it appears to play important roles in anti-mycobacterial immune defenses because knockout mice are more susceptible to this infection (98)”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [98]

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Authors
Mayer-Barber, K. D., Andrade, B. B., Barber, D. L., Hieny, S., Feng, C. G., Caspar, P., Oland, S., Gordon, S., & Sher, A.
Affiliations
  • National Institutes of Health (US)
  • University of Oxford (GB)
Corresponding author
  • Mayer-Barber, Katrin D.
  • Sher, Alan
Venue
Immunity
Publisher
Elsevier BV
Published
2011-12
Volume
35
Issue
6
Pages
1023-1034
ISSN
1074-7613 (ISSN-L)
OpenAlex
W2023478821
Cited by
418
References
48
Citations by year
2026: 16 · 2025: 26 · 2024: 25 · 2023: 31 · 2022: 33 · 2021: 18 · 2020: 27 · 2019: 31 · 2018: 23 · 2017: 31 · 2016: 38 · 2015: 37 · 2014: 31 · 2013: 37 · 2012: 14
FWCI
17.77
Type
journal article
Language
en
Open access
Locations
  • Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (Z99 AI999999)
  • National Cancer Institute
  • National Institute of Allergy and Infectious Diseases (Y99 AI999999)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Keywords
Mycobacterium tuberculosis infection, interleukin-1 alpha, IL-1β, type I interferon, innate immunity, adaptive immunity, monocytes/macrophages, dendritic cells, host resistance, IL-1 signaling, single-cell analysis
MeSH terms
Animals, Antigens, Ly, Dendritic Cells, Humans, Interferons, Lung, Mice, Inbred C57BL, Mycobacterium tuberculosis, Phagocytes, Tuberculosis, Pulmonary, Signal Transduction, CD4-Positive T-Lymphocytes, Mice, Knockout, Myeloid Cells, CD11b Antigen, Mice, Interleukin-1alpha, Interleukin-1beta, Interleukin-12 Subunit p40

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