ReviewSeminars in immunology2014
Cell death and autophagy in tuberculosis.
Review in Seminars in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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
55 citing papers in PubMed.
- NR4A nuclear receptor expression in human macrophages mediates apoptosis and controls Mycobacterium tuberculosis growth.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- A granulin-positive macrophage subtype in mycobacterial granulomas alleviates tissue damage by limiting excessive inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- How macrophage heterogeneity affects tuberculosis disease and therapy.Nature reviews. Immunology · 2025Review
- Identification and Validation of Genes Related to Macrophage Polarization and Cell Death Modes UnderJournal of inflammation research · 2024Article
- Necroptosis in bacterial infections.Frontiers in immunology · 2024Review
- Article
- Combination of MCL-1 and BCL-2 inhibitors is a promising approach for a host-directed therapy for tuberculosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Immunohistochemical Characterization of M1, M2, and M4 Macrophages in Leprosy Skin Lesions.Pathogens (Basel, Switzerland) · 2023Article
- Review
- Role of C-terminal domain of Mycobacterium tuberculosis PE6 (Rv0335c) protein in host mitochondrial stress and macrophage apoptosis.Apoptosis : an international journal on programmed cell death · 2023Article
- Comparative proteome analysis revealed the differences in response to bothFrontiers in cellular and infection microbiology · 2023Article
- Immunological Interactions between Intestinal Helminth Infections and Tuberculosis.Diagnostics (Basel, Switzerland) · 2022Review
- Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022Review
- Regulated necrosis, a proinflammatory cell death, potentially counteracts pathogenic infections.Cell death & disease · 2022Review
- Review
- SCARF1-Induced Efferocytosis Plays an Immunomodulatory Role in Humans, and Autoantibodies Targeting SCARF1 Are Produced in Patients with Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Virulence-Associated Secretion inFrontiers in immunology · 2022Review
- Effects of propofol on macrophage activation and function in diseases.Frontiers in pharmacology · 2022Review
- A Dual Role of Heme Oxygenase-1 in Tuberculosis.Frontiers in immunology · 2022Review
- Down-regulation of hsa_circ_0045474 induces macrophage autophagy in tuberculosis via miR-582-5p/TNKS2 axis.Innate immunity · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Mycobacterium tuberculosis has succeeded in infecting one-third of the human race though inhibition or evasion of innate and adaptive immunity. The pathogen is a facultative intracellular parasite that uses the niche provided by mononuclear phagocytes for its advantage. Complex interactions determine whether the bacillus will or will not be delivered to acidified lysosomes, whether the host phagocyte will survive infection or die, and whether the timing and mode of cell death works to the advantage of the host or the pathogen. Here we discuss cell death and autophagy in TB. These fundamental processes of cell biology feature in all aspects of TB pathogenesis and may be exploited to the treatment or prevention of TB disease.
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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.