ArticleFrontiers in immunology2011
Macrophage polarization: convergence point targeted by mycobacterium tuberculosis and HIV.
Article in Frontiers in immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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.
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.
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Who cites it
58 citing papers in PubMed, 111 citations in OpenAlex.
- L-arginine and vitamin D adjunctive therapies in pulmonary tuberculosis: a randomised, double-blind, placebo-controlled trial.PloS one · 2013Trial
- Macrophage Plasticity: Phenotypic and Functional Profiles Across Pathological Microenvironments.International journal of molecular sciences · 2026Review
- Glycolysis inhibition in tuberculosis-driven metabolic rewiring reduces HIV-1 spread in macrophages.Life science alliance · 2026Article
- The role and mechanisms of multiple immunoregulatory cells in pulmonary tuberculosis.Frontiers in immunology · 2026Review
- Comparative Study of [Molecular imaging and biology · 2025Article
- Monkeypox Virus Subverts the Inflammatory Response of Macrophages at the Maternal-Fetal Interface.Journal of medical virology · 2025Article
- Systemic vasculitis with latent tuberculosis infection and associated factors: a cross-sectional multicenter study.Clinical rheumatology · 2025Article
- Review
- Paired ATAC- and RNA-seq offer insight into the impact of HIV on alveolar macrophages: a pilot study.Scientific reports · 2023Article
- Productive HIV-1 infection of tissue macrophages by fusion with infected CD4+ T cells.The Journal of cell biology · 2023Article
- Article
- Streptococcus suis Serotype 2 Infection Induces Splenomegaly with Splenocyte Apoptosis.Microbiology spectrum · 2022Article
- Mycobacterium intracellulare induces a Th17 immune response via M1-like macrophage polarization in canine peripheral blood mononuclear cells.Scientific reports · 2022Article
- Sp1 transcription factor represses transcription of phosphatase and tensin homolog to aggravate lung injury in mice with type 2 diabetes mellitus-pulmonary tuberculosis.Bioengineered · 2022Article
- The Impact of Alcohol Use Disorder on Tuberculosis: A Review of the Epidemiology and Potential Immunologic Mechanisms.Frontiers in immunology · 2022Review
- Advances in molecular mechanisms of interaction betweenTranslational lung cancer research · 2021Review
- Helminth species specific expansion and increased TNF-alpha production of non-classical monocytes during active tuberculosis.PLoS neglected tropical diseases · 2021Article
- Human monocyte-derived macrophage responses to M. tuberculosis differ by the host's tuberculosis, diabetes or obesity status, and are enhanced by rapamycin.Tuberculosis (Edinburgh, Scotland) · 2021Article
- HIV and the tuberculosis "set point": how HIV impairs alveolar macrophage responses to tuberculosis and sets the stage for progressive disease.Retrovirology · 2020Review
- Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection.Nature communications · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the arms race of host-microbe co-evolution, macrophages (Mɸs) have been endowed with strategies to neutralize pathogenic challenge while preserving host integrity. During steady-states conditions, Mɸs perform multiple house-keeping functions governed by their differentiation state, tissue distribution, and signals from the microenvironment. In response to pathogenic challenge and host mediators, however, Mɸs undergo different programs of activation rendering them either pro-inflammatory and microbicidal (M1), or immunosuppressants and tissue repairers (M2). An excessive or prolonged polarization of either program may be detrimental to the host due to potential tissue injury or contribution to pathogenesis. Conversely, intracellular microbes that cause chronic diseases such as tuberculosis and acquired immunodeficiency syndrome exemplify strategies for survival in the host. Indeed, both Mycobacterium tuberculosis (Mtb) and human immunodeficiency virus (HIV-1) are successful intracellular microbes that thrive in Mɸs. Given these microbes not only co-circulate throughout the developing world but each has contributed to prevalence and mortality caused by the other, substantial insights into microbe physiology and host defenses then rest in the attempt to fully understand their influence on Mɸ polarization. This review addresses the role of Mɸ polarization in the immune response to, and pathogenesis of, Mtb and HIV.
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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.