ArticleJournal of tropical medicine2012
Host cell signalling and leishmania mechanisms of evasion.
Article in Journal of tropical medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 98 citations in OpenAlex.
- Trial
- Concomitant immunity in persistent Leishmania infections: could it represent an evolutionary balance and a vaccine target?Parasites & vectors · 2025Review
- Immune subversion by Leishmania infantum parasites suppresses NLRP3-driven inflammatory responses in amyloid-β-activated microglia.Journal of neuroinflammation · 2025Article
- Glycomics in Human Diseases and Its Emerging Role in Biomarker Discovery.Biomedicines · 2025Review
- An inclusive assessment of apoptosis mechanisms inCurrent research in parasitology & vector-borne diseases · 2025Review
- Activation Pathways of Murine Macrophages by Lipophosphoglycan from Strains ofACS infectious diseases · 2024Article
- Advances inPathogens (Basel, Switzerland) · 2024Review
- Modulation of Macrophage Redox and Apoptotic Processes toPathogens (Basel, Switzerland) · 2023Article
- Comprehensive proteomic analysis of autophagosomes derived from Leishmania-infected macrophages.PloS one · 2023Article
- Epigenetic paradigms/exemplars of the macrophage: inflammasome axis in Leishmaniasis.Molecular and cellular biochemistry · 2022Review
- A Novel Role of Secretory Cytosolic Tryparedoxin Peroxidase in Delaying Apoptosis ofMolecular and cellular biology · 2022Article
- Revisiting Leishmania GP63 host cell targets reveals a limited spectrum of substrates.PLoS pathogens · 2022Article
- Transcriptomic Profile of Canine DH82 Macrophages Infected byInternational journal of molecular sciences · 2022Article
- TLR2 dimer-specific ligands selectively activate protein kinase C isoforms in Leishmania infection.Immunology · 2021Article
- Proteomic Analysis ofPathogens (Basel, Switzerland) · 2021Article
- Clinical Significance of ROMs, OXY, SHp and HMGB-1 in Canine Leishmaniosis.Animals : an open access journal from MDPI · 2021Article
- Insights intoVeterinary sciences · 2021Review
- Modulation of Host Immune Response duringFrontiers in immunology · 2021Article
- Involvement ofFrontiers in cellular and infection microbiology · 2021Review
- Macrophages as host, effector and immunoregulatory cells in leishmaniasis: Impact of tissue micro-environment and metabolism.Cytokine: X · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leishmania parasites are able to secure their survival and propagation within their host by altering signalling pathways involved in the ability of macrophages to kill pathogens or to engage adaptive immune system. An important step in this immune evasion process is the activation of host protein tyrosine phosphatase SHP-1 by Leishmania. SHP-1 has been shown to directly inactivate JAK2 and Erk1/2 and to play a role in the negative regulation of several transcription factors involved in macrophage activation. These signalling alterations contribute to the inactivation of critical macrophage functions (e.g., Nitric oxide, IL-12, and TNF-α). Additionally, to interfere with IFN-γ receptor signalling, Leishmania also alters several LPS-mediated responses. Recent findings from our laboratory revealed a pivotal role for SHP-1 in the inhibition of TLR-induced macrophage activation through binding to and inactivating IL-1-receptor-associated kinase 1 (IRAK-1). Furthermore, we identified the binding site as an evolutionarily conserved ITIM-like motif, which we named kinase tyrosine-based inhibitory motif (KTIM). Collectively, a better understanding of the evasion mechanisms utilized by Leishmania parasite could help to develop more efficient antileishmanial therapies in the near future.
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.