ArticleThe Journal of biological chemistry
IL-4Rα signaling by CD8α
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Microglial tunneling nanotubes: an intercellular transfer facilitating mitochondrial dysfunction and neuroinflammation in experimental cerebral malaria.Apoptosis : an international journal on programmed cell death · 2026Article
- Inhibition ofBiomedicines · 2025Article
- Interleukin-4 and its receptor alpha in paediatric uncomplicated malaria patients from a Ghanaian case-control study.BMC research notes · 2024Article
- Article
- Cytokine gene polymorphisms implicated in the pathogenesis ofFrontiers in immunology · 2024Review
- Potential Benefits of Lycopene Consumption: Rationale for Using It as an Adjuvant Treatment for Malaria Patients and in Several Diseases.Nutrients · 2022Review
- Cerebral Malaria: Current Clinical and Immunological Aspects.Frontiers in immunology · 2022Review
- Recent Advances in Understanding the Inflammatory Response in Malaria: A Review of the Dual Role of Cytokines.Journal of immunology research · 2021Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Persistent high levels of proinflammatory and Th1 responses contribute to cerebral malaria (CM). Suppression of inflammatory responses and promotion of Th2 responses prevent pathogenesis. IL-4 commonly promotes Th2 responses and inhibits inflammatory and Th1 responses. Therefore, IL-4 is widely considered as a beneficial cytokine via its Th2-promoting role that is predicted to provide protection against severe malaria by inhibiting inflammatory responses. However, IL-4 may also induce inflammatory responses, as the result of IL-4 action depends on the timing and levels of its production and the tissue environment in which it is produced. Recently, we showed that dendritic cells (DCs) produce IL-4 early during malaria infection in response to a parasite protein and that this IL-4 response may contribute to severe malaria. However, the mechanism by which IL-4 produced by DCs contributing to lethal malaria is unknown. Using Plasmodium berghei ANKA-infected C57BL/6 mice, a CM model, we show here that mice lacking IL-4Rα only in CD8α
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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.