ArticleJournal of immunology (Baltimore, Md. : 1950)2009
IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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Who cites it
118 citing papers in PubMed, 230 citations in OpenAlex.
- Enhancing Preclinical Rigor: Evaluating Robustness and Numerical Stability in a Chronic Pancreatitis Mouse Model.Annals of the New York Academy of Sciences · 2026Article
- Leishmania Extracellular Vesicles as a Preventive Vaccine Platform Against Leishmaniasis.Journal of extracellular vesicles · 2026Article
- Revisiting the past in light of current knowledge on γδ T cells in leishmaniasis.Frontiers in immunology · 2026Review
- An overview of host immune responses against Leishmania spp. infections.Human molecular genetics · 2025Review
- Staphylococcus aureus promotes strain-dependent immunopathology during cutaneous leishmaniasis through induction of IL-1β.Cell reports · 2025Article
- Non-additive strong gene interactions cause striking differences in organ pathology and cytokine response in Leishmaniasis.Frontiers in immunology · 2025Article
- Mice mucosal leishmaniasis model shown high parasite load, increased cytotoxicity and impaired IL-10Frontiers in immunology · 2025Article
- Improving reproducibility and translational potential of mouse models: lessons from studying leishmaniasis.Frontiers in immunology · 2025Review
- Chemokines Signature and T Cell Dynamics in Leishmaniasis: Molecular insight and therapeutic application.Expert reviews in molecular medicine · 2024Review
- Role of neutrophils in the pathogenesis of Post Kala-azar Dermal Leishmaniasis (PKDL).PLoS neglected tropical diseases · 2024Article
- An integrated bioinformatic analysis of microarray datasets to identify biomarkers and miRNA-based regulatory networks in leishmaniasis.Scientific reports · 2024Article
- Heterologous Expression of Human IFNγ and Anti-IL17 Antibody in Leishmania tarentolae Promastigote.Acta parasitologica · 2024Article
- Th17 Cell and Inflammatory Infiltrate Interactions in Cutaneous Leishmaniasis: Unraveling Immunopathogenic Mechanisms.Immune network · 2024Review
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- Memory T cells: promising biomarkers for evaluating protection and vaccine efficacy against leishmaniasis.Frontiers in immunology · 2024Review
- Regulatory T cells control Staphylococcus aureus and disease severity of cutaneous leishmaniasis.The Journal of experimental medicine · 2023Article
- Deletion of MIF gene from live attenuated LdCenScientific reports · 2023Article
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- Leishmania major Strain-Dependent Macrophage Activation Contributes to Pathogenicity in the Absence of Lymphocytes.Microbiology spectrum · 2022Article
58 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
6 authors at 3 institutions in 4 countries.
Funding
Abstract
Resistance to leishmaniasis in C57BL/6 mice depends on Th1/Tc1 cells. BALB/c mice preferentially develop Th2 immunity and succumb to infection. We now assessed the role of IL-17 in cutaneous leishmaniasis. During the course of Leishmania major infection, BALB/c CD4 cells and neutrophils produced increased amounts of IL-17 as compared with cells from C57BL/6 mice. This increase was associated with significantly increased IL-23 release from L. major-infected BALB/c dendritic cells (DC), whereas IL-6 and TGF-beta1 production by BALB/c and C57BL/6 DC were comparable. Interestingly, lesion sizes in infected IL-17-deficient BALB/c mice were dramatically smaller and failed to progress as compared with those in control mice. Similar amounts of IL-4, IL-10, and IFN-gamma were produced by T cells from IL-17-deficient mice and control mice consistent with development of Th2-predominant immunity in all animals. Improved disease outcome was associated with decreased CXCL2-accumulation in lesion sites and decreased neutrophil immigration into lesions of infected IL-17-deficient mice confirming prior observations that enhanced neutrophil recruitment contributes to disease susceptibility in BALB/c mice. This study excludes an important facilitating role for IL-17 in Th1/Th2 development in L. major-infected BALB/c mice, and suggests that IL-23 production by L. major-infected DC maintains IL-17(+) cells that influence disease progression via regulation of neutrophil recruitment.
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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.