ArticleCell reports2023
Single-cell analysis reveals a weak macrophage subpopulation response to Mycobacterium tuberculosis infection.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Article
- Bacterial surface display enables lysis-independent joint host-pathogen single-cell profiling.bioRxiv : the preprint server for biology · 2026Article
- IFN-γ and IL-17 elicit synergistic anti-mycobacterial responses by inhibiting coronin-1A retention.Communications biology · 2025Article
- Scutellarin suppresses Mycobacterium tuberculosis-induced pyroptosis in macrophages by inhibiting the HIF-1α-mediated Warburg effect.Redox report : communications in free radical research · 2025Article
- Article
- Proximity labeling defines the phagosome lumen proteome of murine and primary human macrophages.bioRxiv : the preprint server for biology · 2024Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) infection remains one of society's greatest human health challenges. Macrophages integrate multiple signals derived from ontogeny, infection, and the environment. This integration proceeds heterogeneously during infection. Some macrophages are infected, while others are not; therefore, bulk approaches mask the subpopulation dynamics. We establish a modular, targeted, single-cell protein analysis framework to study the immune response to Mtb. We demonstrate that during Mtb infection, only a small fraction of resting macrophages produce tumor necrosis factor (TNF) protein. We demonstrate that Mtb infection results in muted phosphorylation of p38 and JNK, regulators of inflammation, and leverage our single-cell methods to distinguish between pathogen-mediated interference in host signaling and weak activation of host pathways. We demonstrate that the inflammatory signal magnitude is decoupled from the ability to control Mtb growth. These data underscore the importance of developing pathogen-specific models of signaling and highlight barriers to activation of pathways that control inflammation.
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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.