ArticleNature immunology2010
Eicosanoid pathways regulate adaptive immunity to Mycobacterium tuberculosis.
Article in Nature immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
140 citing papers in PubMed, 2 syntheses or guidelines pooled it, 246 citations in OpenAlex.
- Delayed-Type Hypersensitivity toInternational journal of molecular sciences · 2026Pooled it
- Systematic review of innate immune responses againstFrontiers in immunology · 2024Pooled it
- Plasma LOX-Products and Monocyte Signaling Is Reduced by Adjunctive Cyclooxygenase-2 Inhibitor in a Phase I Clinical Trial of Tuberculosis Patients.Frontiers in cellular and infection microbiology · 2021Trial
- Host-pathogen interactions in tuberculosis: from immunological mechanisms to translational applications.Cell insight · 2026Review
- Host eicosanoid signals define a granuloma fibroblast population that coordinates mycobacterial containment.Cell host & microbe · 2026Article
- Inhalational therapy of pulmonary infectionActa pharmaceutica Sinica. B · 2026Article
- Immunodominant Tuberculosis Antigens Recognized by Human CD4Cold Spring Harbor perspectives in medicine · 2026Article
- BHLHE40 contributes to allergic asthma progression in mice through NRTN downregulation in macrophages.Communications biology · 2025Article
- Epigenetic regulation of hematopoietic stem cell fate.Trends in cell biology · 2025Review
- Microenvironments of tuberculous granuloma: advances and opportunities for therapy.Frontiers in immunology · 2025Review
- CD4International journal of molecular sciences · 2024Article
- Efferocytosis in dendritic cells: an overlooked immunoregulatory process.Frontiers in immunology · 2024Review
- Understanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.Frontiers in immunology · 2024Review
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- High Bacillary Burden and the ESX-1 Type VII Secretion System Promote MHC Class I Presentation by Mycobacterium tuberculosis-Infected Macrophages to CD8 T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Autophagy restricts Mycobacterium tuberculosis during acute infection in mice.Nature microbiology · 2023Article
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80 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The fate of infected macrophages has an essential role in protection against Mycobacterium tuberculosis by regulating innate and adaptive immunity. M. tuberculosis exploits cell necrosis to exit from macrophages and spread. In contrast, apoptosis, which is characterized by an intact plasma membrane, is an innate mechanism that results in lower bacterial viability. Virulent M. tuberculosis inhibits apoptosis and promotes necrotic cell death by inhibiting production of prostaglandin E(2). Here we show that by activating the 5-lipoxygenase pathway, M. tuberculosis not only inhibited apoptosis but also prevented cross-presentation of its antigens by dendritic cells, which impeded the initiation of T cell immunity. Our results explain why T cell priming in response to M. tuberculosis is delayed and emphasize the importance of early immunity.
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What OpenQuestion holds
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.