ArticleJournal of cell science2023
Src- and Abl-family kinases activate spleen tyrosine kinase to maximize phagocytosis and Leishmania infection.
Article in Journal of cell science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 8 citations in OpenAlex.
- DNA Methylation in macrophages infected withEmerging microbes & infections · 2025Article
- Integrated transcriptomic and immune enzymatic analyses uncover coordinated immunometabolic responses in large yellow croaker (Frontiers in immunology · 2025Article
- Using machine learning to dissect host kinases required for Leishmania internalization and development.Molecular and biochemical parasitology · 2024Article
- Using machine learning to dissect host kinases required forbioRxiv : the preprint server for biology · 2024Article
- A Multi-Color Immunofluorescence Assay to Distinguish Intracellular From ExternalBio-protocol · 2024Article
- MAPK/ERK activation in macrophages promotes Leishmania internalization and pathogenesis.Microbes and infectionArticle
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Leishmania spp. are obligate intracellular parasites that must be internalized by phagocytic cells to evade immune responses and cause disease. The uptake of both Leishmania promastigotes (insect-stage parasites) and amastigotes (proliferative-stage parasites in humans and mice) by phagocytes is thought to be mainly host cell driven, not parasite driven. Our previous work indicates that host Src- and Abl-family kinases facilitate Leishmania entry into macrophages and pathogenesis in murine cutaneous leishmaniasis. Here, we demonstrate that host spleen tyrosine kinase (SYK) is required for efficient uptake of Leishmania promastigotes and amastigotes. A Src-family kinase-Abl-family kinase-SYK signaling cascade induces Leishmania amastigote internalization. Finally, lesion size and parasite burden during Leishmania infection is significantly decreased in mice lacking SYK in monocytes or by treatment with the SYK inhibitor entospletinib. In summary, SYK is required for maximal Leishmania uptake by macrophages and disease in mice. Our results suggest potential for treating leishmaniasis using host cell-directed agents.
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Registered trials
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