ArticleClinical & developmental immunology2012
Characterization of chronic cutaneous lesions from TNF-receptor-1-deficient mice infected by Leishmania major.
Article in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Article
- Natural Products: Insights into Leishmaniasis Inflammatory Response.Mediators of inflammation · 2015Review
- Impairment of T cell function in parasitic infections.PLoS neglected tropical diseases · 2014Review
- Engagement of NKG2D on bystander memory CD8 T cells promotes increased immunopathology following Leishmania major infection.PLoS pathogens · 2014Article
- Leishmania major Self-Limited Infection Increases Blood Cholesterol and Promotes Atherosclerosis Development.Cholesterol · 2013Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leishmania major-infected TNF receptor 1 deficient (TNFR1 KO) mice resolve parasitism but fail to resolve lesions, while wild-type mice completely heal. We investigated the cell composition, cytokine production, and apoptosis in lesions from L. major-infected TNFR1 KO and wild-type (WT) mice. Chronic lesions from L. major-infected TNFR1 KO mice presented larger number of CD8+ T and Ly6G+ cells. In addition, higher concentrations of mRNA for IFN-γ CCL2 and CCL5, as well as protein, but lower numbers of apoptotic cells, were found in lesions from TNFR1 KO mice than in WT, at late time points of infection. Our studies showed that persistent lesions in L. major-infected TNFR1 KO mice may be mediated by continuous migration of cells to the site of inflammation due to the presence of chemokines and also by lower levels of apoptosis. We suggest that this model has some striking similarities to the mucocutaneous clinical form of leishmaniasis.
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Registered trials
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