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

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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, Sher, Alan·2011·Immunity

DOI 10.1016/j.immuni.2011.12.002PMC PMC3246221

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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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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
ORCID: Mayer-Barber, Katrin D.
Andrade, Bruno B.
Barber, Daniel L.
Feng, Carl G.
Gordon, Siamon
Sher, Alan
Venue: Immunity
Publisher: Elsevier BV
Published: 2011-12
Volume: 35
Issue: 6
Pages: 1023-1034
ISSN: 1074-7613 (ISSN-L)
DOI: 10.1016/j.immuni.2011.12.002
PMC: PMC3246221
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: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 594 d)
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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Innate and Adaptive Interferons Suppress IL-1α and IL-1β Production by Distinct Pulmonary Myeloid Subsets during Mycobacterium tuberculosis Infection

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