ArticleJournal of leukocyte biology2014
Inhibition of caspase-8 activity promotes protective Th1- and Th2-mediated immunity to Leishmania major infection.
Article in Journal of leukocyte biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 8 citations in OpenAlex.
- Caspase-8 expression in CD8Science advances · 2025Article
- Targeting macrophage phenotypes to prevent diseases caused byFrontiers in immunology · 2025Review
- New Therapeutic Tools to Shape Monocyte Functional Phenotypes in Leishmaniasis.Frontiers in immunology · 2021Review
- Toll-Like Receptor and miRNA-let-7e Expression Alter the Inflammatory Response inFrontiers in immunology · 2018Article
- Association between angiogenesis and cytotoxic signatures in the tumor microenvironment of gastric cancer.OncoTargets and therapy · 2018Article
- All-Frontiers in immunology · 2017Article
- Innate immunity to Leishmania infection: within phagocytes.Mediators of inflammation · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
We investigated how apoptosis pathways mediated by death receptors and caspase-8 affect cytokine responses and immunity to Leishmania major parasites. Splenic CD4 T cells undergo activation-induced apoptosis, and blockade of FasL-Fas interaction increased IFN-γ and IL-4 cytokine responses to L. major antigens. To block death receptor-induced death, we used mice expressing a T cell-restricted transgene for vFLIP. Inhibition of caspase-8 activation in vFLIP mice enhanced Th1 and Th2 cytokine responses to L. major infection, even in the Th1-prone B6 background. We also observed increased NO production by splenocytes from vFLIP mice upon T cell activation. Despite an exacerbated Th2 response, vFLIP mice controlled better L. major infection, with reduced lesions and lower parasite loads compared with WT mice. Moreover, injection of anti-IL-4 mAb in infected vFLIP mice disrupted control of parasite infection. Therefore, blockade of caspase-8 activity in T cells improves immunity to L. major infection by promoting increased Th1 and Th2 responses.
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Registered trials
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