ArticleProceedings of the National Academy of Sciences of the United States of America2015
IL-1R signaling enables bystander cells to overcome bacterial blockade of host protein synthesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 78 citations in OpenAlex.
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- Absence of c-Maf and IL-10 enables type I IFN enhancement of innate responses to LPS in alveolar macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
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- An IFNγ-dependent immune-endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response.Nature immunology · 2024Article
- Absence of c-Maf and IL-10 enables Type I IFN enhancement of innate responses to low-dose LPS in alveolar macrophages.bioRxiv : the preprint server for biology · 2024Article
- A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas.The Journal of experimental medicine · 2024Article
- TLR9-independent CD8Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Single-cell analysis reveals a weak macrophage subpopulation response to Mycobacterium tuberculosis infection.Cell reports · 2023Article
- TNF licenses macrophages to undergo rapid caspase-1, -11, and -8-mediated cell death that restricts Legionella pneumophila infection.PLoS pathogens · 2023Article
- Hiding in the yolk: A unique feature of Legionella pneumophila infection of zebrafish.PLoS pathogens · 2023Article
- A TNF-IL-1 circuit controlsbioRxiv : the preprint server for biology · 2023Article
- Cigarette smoke depletes alveolar macrophages and delays clearance ofAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- Interaction between alveolar macrophages and epithelial cells duringFrontiers in cellular and infection microbiology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The innate immune system is critical for host defense against microbial pathogens, yet many pathogens express virulence factors that impair immune function. Here, we used the bacterial pathogen Legionella pneumophila to understand how the immune system successfully overcomes pathogen subversion mechanisms. L. pneumophila replicates within macrophages by using a type IV secretion system to translocate bacterial effectors into the host cell cytosol. As a consequence of effector delivery, host protein synthesis is blocked at several steps, including translation initiation and elongation. Despite this translation block, infected cells robustly produce proinflammatory cytokines, but the basis for this is poorly understood. By using a reporter system that specifically discriminates between infected and uninfected cells within a population, we demonstrate here that infected macrophages produced IL-1α and IL-1β, but were poor producers of IL-6, TNF, and IL-12, which are critical mediators of host protection. Uninfected bystander cells robustly produced IL-6, TNF, and IL-12, and this bystander response required IL-1 receptor (IL-1R) signaling during early pulmonary infection. Our data demonstrate functional heterogeneity in production of critical protective cytokines and suggest that collaboration between infected and uninfected cells enables the immune system to bypass pathogen-mediated translation inhibition to generate an effective immune response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.