ReviewClinical microbiology reviews2005
Subversion mechanisms by which Leishmania parasites can escape the host immune response: a signaling point of view.
Review in Clinical microbiology reviews, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 1 of them a synthesis 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
212 citing papers in PubMed, 1 synthesis or guideline pooled it, 487 citations in OpenAlex.
- Integrative transcriptomics and hypothesis-driven transfer machine learning reveal conserved and species-specific host-parasite dynamics acrossFrontiers in cellular and infection microbiology · 2026Pooled it
- Delayed fractional dose regimen of the RTS,S/AS01 malaria vaccine candidate enhances an IgG4 response that inhibits serum opsonophagocytosis.Scientific reports · 2017Trial
- Immune-mediated remodelling of tissue architecture in Post-Kala-Azar Dermal Leishmaniasis (PKDL).PLoS neglected tropical diseases · 2026Article
- Comparative RNA-Seq Analysis Reveals Macrophage Polarization and T Cell Exhaustion Signatures in Visceral Leishmaniasis.International journal of molecular sciences · 2026Article
- Development of DNA Aptamers AgainstPharmaceutics · 2026Article
- Review on macrophage polarization during visceral leishmaniasis and impact of glycoprotein.Glycoconjugate journal · 2026Review
- Leishmaniasis: pathogenesis, host immunity, and the evolving landscape of immunotherapy and immunochemotherapy.Frontiers in microbiology · 2026Review
- Natural product-based therapeutic strategies againstFrontiers in microbiology · 2026Review
- Development of a High-Throughput Screening Platform and a Pathogenesis Model forInternational journal of molecular sciences · 2025Article
- Immune subversion by Leishmania infantum parasites suppresses NLRP3-driven inflammatory responses in amyloid-β-activated microglia.Journal of neuroinflammation · 2025Article
- An overview of host immune responses against Leishmania spp. infections.Human molecular genetics · 2025Review
- Review
- Cytokine Networks and the Clinical Outcome of American Teg-Umentary Leishmaniasis: Unveiling Targets for Alternative Therapeutic Interventions.Pathogens (Basel, Switzerland) · 2025Review
- The Potential Role of Sanguinarine as an Inhibitor of Leishmania PP2C in the Induction of Apoptosis.Acta parasitologica · 2025Article
- FcRγIIA attenuates pathology of cutaneous leishmaniasis and modulates ITAMa/i balance.Parasites & vectors · 2024Article
- Expression of Network Medicine-Predicted Genes in Human Macrophages Infected withInternational journal of molecular sciences · 2024Article
- The Immune Memory Response of In Vitro-Polarised Th1, Th2, and Th17 Cells in the Face of Ovalbumin-TransgenicInternational journal of molecular sciences · 2024Article
- Human Dendritic Cell Maturation Is Modulated byTropical medicine and infectious disease · 2024Article
- The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses.International journal of molecular sciences · 2024Review
- Memory T cells: promising biomarkers for evaluating protection and vaccine efficacy against leishmaniasis.Frontiers in immunology · 2024Review
152 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The obligate intracellular parasite Leishmania must survive the antimicrobial activities of its host cell, the macrophage, and prevent activation of an effective immune response. In order to do this, it has developed numerous highly successful strategies for manipulating activities, including antigen presentation, nitric oxide and oxygen radical generation, and cytokine production. This is generally the result of interactions between Leishmania cell surface molecules, particularly gp63 and LPG, and less well identified macrophage surface receptors, causing the distortion of specific intracellular signaling cascades. We describe some of the signaling pathways and intermediates that are repressed in infected cells, including JAK/STAT, Ca(2+)-dependent protein kinase C (PKC) isoforms, and mitogen-activated protein kinases (especially ERK1/2), and proteasome-mediated transcription factor degradation. We also discuss protein tyrosine phosphatases (particularly SHP-1), intracellular Ca2+, Ca(2+)-independent PKC, ceramide, and the suppressors of cytokine signaling family of repressors, which are all reported to be activated following infection, and the role of parasite-secreted cysteine proteases.
Indexed as
Identifiers
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.