ReviewSeminars in immunopathology2018
Macrophage-microbe interaction: lessons learned from the pathogen Mycobacterium tuberculosis.
Review in Seminars in immunopathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- Copper Metabolism in Isolated Macrophages: Regulator of Immunity and Inflammation.Veterinary sciences · 2026Review
- Article
- Cell death pathways in response toInfection and immunity · 2025Review
- NapR Regulates the Expression of Phosphoserine Aminotransferase SerC to Modulate Biofilm Formation and Resistance to Serine Stress of Mycobacteria.International journal of molecular sciences · 2025Article
- Insufficient CXCL13 secretion in leprosy foamy macrophages attenuates lymphocyte recruitment and antimicrobial protein production.Frontiers in immunology · 2025Article
- Differential Host Gene Expression in Response to Infection by DifferentMicroorganisms · 2024Article
- Statistical and network analyses reveal mechanisms for the enhancement of macrophage immunity by manganese inBiochemistry and biophysics reports · 2024Article
- The Role of Rv1476 in Regulating Stress Response and Intracellular Survival ofCurrent issues in molecular biology · 2024Article
- Mechanisms of lung damage in tuberculosis: implications for chronic obstructive pulmonary disease.Frontiers in cellular and infection microbiology · 2023Review
- Review
- MiR-25 blunts autophagy and promotes the survival ofiScience · 2022Article
- Up-regulated SAMD9L modulated by TLR2 and HIF-1α as a promising biomarker in tuberculosis.Journal of cellular and molecular medicine · 2022Article
- The Role of TLR2 in Infectious Diseases Caused by Mycobacteria: From Cell Biology to Therapeutic Target.Biology · 2022Review
- Study on the Correlation between Interleukin-27 and CXCL10 in Pulmonary Tuberculosis.Journal of immunology research · 2022Article
- Integrative genomics of the mammalian alveolar macrophage response to intracellular mycobacteria.BMC genomics · 2021Article
- PRAK Promotes the Pathogen Clearance by Macrophage Through Regulating Autophagy and Inflammasome Activation.Frontiers in immunology · 2021Article
- Promotion of Anti-Tuberculosis Macrophage Activity by L-Arginine in the Absence of Nitric Oxide.Frontiers in immunology · 2021Article
- Survival in Hostile Conditions: Pupylation and the Proteasome in Actinobacterial Stress Response Pathways.Frontiers in molecular biosciences · 2021Review
- mtROS InducedFrontiers in immunology · 2021Article
- Antimicrobial Activity of Neutrophils Against Mycobacteria.Frontiers in immunology · 2021Review
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
No grant is acknowledged in the PubMed record.
Abstract
Macrophages, being the cornerstone of the immune system, have adapted the ancient nutrient acquisition mechanism of phagocytosis to engulf various infectious organisms thereby helping to orchestrate an appropriate host response. Phagocytosis refers to the process of internalization and degradation of particulate material, damaged and senescent cells and microorganisms by specialized cells, after which the vesicle containing the ingested particle, the phagosome, matures into acidic phagolysosomes upon fusion with hydrolytic enzyme-containing lysosomes. The destructive power of the macrophage is further exacerbated through the induction of macrophage activation upon a variety of inflammatory stimuli. Despite being the end-point for many phagocytosed microbes, the macrophage can also serve as an intracellular survival niche for a number of intracellular microorganisms. One microbe that is particularly successful at surviving within macrophages is the pathogen Mycobacterium tuberculosis, which can efficiently manipulate the macrophage at several levels, including modulation of the phagocytic pathway as well as interfering with a number of immune activation pathways that normally would lead to eradication of the internalized bacilli. M. tuberculosis excels at circumventing destruction within macrophages, thus establishing itself successfully for prolonged times within the macrophage. In this contribution, we describe a number of general features of macrophages in the context of their function to clear an infection, and highlight the strategies employed by M. tuberculosis to counter macrophage attack. Interestingly, research on the evasion tactics employed by M. tuberculosis within macrophages not only helps to design strategies to curb tuberculosis, but also allows a better understanding of host cell biology.
Indexed as
Identifiers
30306257What 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.