ArticleInfection and immunity2015
Interleukin-10 from T cells, but not macrophages and granulocytes, is required for chronic disease in Leishmania mexicana infection.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 22 citations in OpenAlex.
- Microneedle-based injection of Fungizone/Amphotericin B: an effective treatment for American cutaneous leishmaniasis in mice.Drug delivery · 2026Article
- Metabolically reprogrammed eosinophils impair T cell immunity and cause chronic skin infection.EMBO molecular medicine · 2026Article
- Mice mucosal leishmaniasis model shown high parasite load, increased cytotoxicity and impaired IL-10Frontiers in immunology · 2025Article
- Article
- Macrophages as host, effector and immunoregulatory cells in leishmaniasis: Impact of tissue micro-environment and metabolism.Cytokine: X · 2020Article
- Nonconventional opponents: a review of malaria and leishmaniasis among United States Armed Forces.PeerJ · 2019Article
- Analysis of the Antigenic and Prophylactic Properties of theFrontiers in cellular and infection microbiology · 2018Article
- The role of the P2X7 receptor in murine cutaneous leishmaniasis: aspects of inflammation and parasite control.Purinergic signalling · 2017Article
- Effects of Bone Marrow Mesenchymal Stromal Cell Therapy in Experimental Cutaneous Leishmaniasis in BALB/c Mice Induced byFrontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
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Abstract
Chronic cutaneous disease of mice caused by the protozoan parasite Leishmania mexicana requires interleukin-10 (IL-10) and FcγRIII (an activating IgG receptor). Macrophages readily secrete IL-10 in response to IgG-coated amastigotes, making macrophages a prime candidate as the critical source of IL-10. However, indirect evidence suggested that macrophage IL-10 is not essential for chronic disease. I now show directly that mice lacking IL-10 from macrophages and granulocytes still have chronic disease, like wild-type C57BL/6 mice. However, T cell-derived IL-10 is required for chronic disease. CD4-cre IL-10flox/flox mice lack IL-10 from T cells (both CD4+ and CD8+) and heal their L. mexicana lesions, with parasite control. I had previously shown that depletion of CD25+ T cells had no effect on chronic disease, and thus, T cells other than CD25+ regulatory T (Treg) cells should be the important source of IL-10. Given that conventional T cells do not express FcγRs, there is likely to be an indirect pathway by which FcγRIII on some other cell engaged by IgG1-amastigote immune complexes induces IL-10 from T cells. Further work is needed to delineate these pathways.
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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.