ArticleCell host & microbe2011
Leishmania promotes its own virulence by inducing expression of the host immune inhibitory ligand CD200.
Article in Cell host & microbe, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 64 citations in OpenAlex.
- Radiation-induced CD200Cellular & molecular immunology · 2026Article
- Leishmania amazonensis impairs phagosome acidification in B-1 phagocytes as an unrecognized parasite infection and proliferation mechanism.Scientific reports · 2025Article
- Transcriptional Profiling ofMicroorganisms · 2022Article
- Transcriptional profiling of macrophages reveals distinct parasite stage-driven signatures during early infection by Leishmania donovani.Scientific reports · 2022Article
- Immune Responses in Leishmaniasis: An Overview.Tropical medicine and infectious disease · 2022Review
- In Silico Characterization of Calcineurin from Pathogenic Obligate Intracellular Trypanosomatids: Potential New Biological Roles.Biomolecules · 2021Article
- The CD200 Regulates Inflammation in Mice Independently of TNF-α Production.International journal of molecular sciences · 2021Article
- Unraveling the Role of Immune Checkpoints in Leishmaniasis.Frontiers in immunology · 2021Review
- Effect of DODAB Nano-Sized Cationic Bilayer Fragments againstMolecules (Basel, Switzerland) · 2020Article
- Programmed Cell Death Ligand (PD-L)-1 Contributes to the Regulation of CD4Frontiers in immunology · 2020Article
- TLR9/MyD88/TRIF signaling activates host immune inhibitory CD200 in Leishmania infection.JCI insight · 2019Article
- CD200 ModulatesInternational journal of molecular sciences · 2019Article
- Quantification of Intracellular Growth Inside Macrophages is a Fast and Reliable Method for Assessing the Virulence of Leishmania Parasites.Journal of visualized experiments : JoVE · 2018Article
- Receptors That Inhibit Macrophage Activation: Mechanisms and Signals of Regulation and Tolerance.Journal of immunology research · 2018Review
- Article
- Review
- Centrin-DeletedFrontiers in immunology · 2018Article
- CD100/Sema4D Increases Macrophage Infection byFrontiers in microbiology · 2018Article
- Quantitative proteomic analysis of amastigotes from Leishmania (L.) amazonensis LV79 and PH8 strains reveals molecular traits associated with the virulence phenotype.PLoS neglected tropical diseases · 2017Article
- The enemy within: Targeting host-parasite interaction for antileishmanial drug discovery.PLoS neglected tropical diseases · 2017Review
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6 authors at 3 institutions in 1 country.
Funding
Abstract
Leishmania parasites infect macrophages, cells normally involved in innate defense against pathogens. Leishmania amazonensis and Leishmania major cause severe or mild disease, respectively, consistent with each parasite's ability to survive within activated macrophages. The mechanisms underlying increased virulence of L. amazonensis are mostly unknown. We show that L. amazonensis promotes its own survival by inducing expression of CD200, an immunoregulatory molecule that inhibits macrophage activation. L. amazonensis does not form typical nonhealing lesions in CD200(-/-) mice and cannot replicate in CD200(-/-) macrophages, an effect reversed by exogenous administration of soluble CD200-Fc. The less virulent L. major does not induce CD200 expression and forms small, self-healing lesions in both wild-type and CD200(-/-) mice. Notably, CD200-Fc injection transforms the course of L. major infection to one resembling L. amazonensis, with large, nonhealing lesions. CD200-dependent iNOS inhibition allows parasite growth in macrophages, identifying a mechanism for the increased virulence of L. amazonensis.
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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.