ArticlePLoS neglected tropical diseases2015
Coinjection with TLR2 agonist Pam3CSK4 reduces the pathology of leishmanization in mice.
Article in PLoS neglected tropical diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Immunotherapeutic Strategies as Potential Treatment Options for Cutaneous Leishmaniasis.Vaccines · 2024Review
- Enhancing Control ofAnimals : an open access journal from MDPI · 2024Article
- Single-cell analysis reveals a weak macrophage subpopulation response to Mycobacterium tuberculosis infection.Cell reports · 2023Article
- Paradoxical immune response in leishmaniasis: The role of toll-like receptors in disease progression.Parasite immunology · 2022Review
- Oral Tolerance Induced by Heat Shock Protein 65-ProducingFrontiers in immunology · 2021Article
- Cross-linking Proteomics Indicates Effects of Simvastatin on the TLR2 Interactome and Reveals ACTR1A as a Novel Regulator of the TLR2 Signal Cascade.Molecular & cellular proteomics : MCP · 2019Article
- TLR2 Signaling in Skin Nonhematopoietic Cells Induces Early Neutrophil Recruitment in Response to Leishmania major Infection.The Journal of investigative dermatology · 2019Article
- CD14 is critical for TLR2-mediated M1 macrophage activation triggered by N-glycan recognition.Scientific reports · 2017Article
- The inflammatory cytokine effect of Pam3CSK4 TLR2 agonist alone or in combination with Leishmania infantum antigen on ex-vivo whole blood from sick and resistant dogs.Parasites & vectors · 2017Article
- Cutaneous Leishmaniasis: Update on Vaccine Development.Human parasitic diseases (Auckland, N.Z.) · 2017Article
- Toll-Like Receptor 2 Is Required for Inflammatory Process Development duringFrontiers in microbiology · 2017Article
- Insights on adaptive and innate immunity in canine leishmaniosis.Parasitology · 2017Article
- Toll-Like Receptor 2 Agonist Pam3CSK4 Alleviates the Pathology of Leptospirosis in Hamster.Infection and immunity · 2016Article
- Gene Expression Profile of High IFN-γ Producers Stimulated with Leishmania braziliensis Identifies Genes Associated with Cutaneous Leishmaniasis.PLoS neglected tropical diseases · 2016Article
- Toll-like receptor 2 (TLR2) plays a role in controlling cutaneous leishmaniasis in vivo, but does not require activation by parasite lipophosphoglycan.Parasites & vectors · 2016Article
- Differences in immune responses against Leishmania induced by infection and by immunization with killed parasite antigen: implications for vaccine discovery.Parasites & vectors · 2016Review
- Interleukin-27 Early ImpactsFrontiers in immunology · 2016Article
- Innate immunity against Leishmania infections.Cellular microbiology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cutaneous leishmaniasis caused by Leishmania major is an emergent, uncontrolled public health problem and there is no vaccine. A promising prophylactic approach has been immunotherapy with Toll-like receptor (TLR) agonists to enhance parasite-specific immune responses. We have previously reported that vaccination of C57BL/6 mice with live L. major plus the TLR9 agonist CpG DNA prevents lesion development and confers immunity to reinfection. Our current study aims to investigate whether other TLR agonists can be used in leishmanization without induction of lesion formation. We found that live L. major plus the TLR2 agonist Pam3CSK4 reduced the pathology in both genetically resistant (C57BL/6) and susceptible (BALB/c) mouse strains. The addition of Pam3CSK4 activated dermal dendritic cells and macrophages to produce greater amounts of proinflammatory cytokines in both mouse strains. Both Th1 and Th17 responses were enhanced by leishmanization with L. major plus Pam3CSK4 in C57BL/6 mice; however, Th17 cells were unchanged in BALB/c mice. The production of IL-17 from neutrophils was enhanced in both strains infected with L. major plus Pam3CSK4. However, the sustained influx of neutrophils in sites of infection was only observed in BALB/c mice. Our data demonstrate that the mechanism behind leishmanization with TLR agonists may be very different depending upon the immunological background of the host. This needs to be taken into account for the rational development of successful vaccines against the disease.
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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.