ArticleFrontiers in immunology2025
Helminthic larval stage induces cellular apoptosis via caspase 9-mediated mitochondrial dysfunction.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Monoclonal antibody-based immunohistochemistry reveals residual Taenia solium antigens in calcified granulomas from pigs with neurocysticercosis.PLoS neglected tropical diseases · 2026Article
- Immunoendocrine Profiles in Neurocysticercosis Patients: A Case-Control Study in Honduras.Tropical medicine and infectious disease · 2026Article
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Authors and funding
16 authors.
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Abstract
Introduction: In human neurocysticercosis (NCC), the cellular and molecular mechanisms of host-parasite interactions triggering brain inflammation and epileptic seizures in Sub-Saharan Africa are poorly understood. Emerging evidence indicates that the viability of the cyst of the pork tapeworm Materials and methods: Human and porcine peripheral immune cells, as well as murine microglia, were exposed to Results: We found that vesicular fluid derived from cysts primarily induced apoptosis and caspase 3 and 9 activity, and only minimal necrosis, in a dose-dependent manner across central and peripheral immune cells. This effect was prominent in CD16 Conclusions: This study identifies caspase 9-mediated apoptosis as a mechanism of helminth-induced brain inflammation and implicates FasL in symptomatic disease progression. These insights enhance our understanding of NCC immunopathogenesis and may inform future therapeutic strategies targeting apoptotic pathways.
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