ArticleJournal of immunology (Baltimore, Md. : 1950)2012
TLR9 and MyD88 are crucial for the development of protective immunity to malaria.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
55 citing papers in PubMed, 87 citations in OpenAlex.
- Overcoming Immune Therapy Resistance in Cancer Through Innate Immune Reprogramming.International journal of molecular sciences · 2025Review
- Immunophenotyping of Hematopoietic Cells in the Spleen in Hypothyroid Mice.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Article
- Interplay of Chemokines Receptors, Toll-like Receptors, and Host Immunological Pathways.Biomedicines · 2023Review
- The ultimate tradeoff: how red cell adaptations to malaria alter the host response during critical illness.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- TLR7 modulates extramedullary splenic erythropoiesis in P. yoelii NSM-infected mice through the regulation of iron metabolism of macrophages with IFN-γ.Frontiers in immunology · 2023Article
- Review
- Recent Advances in Understanding the Inflammatory Response in Malaria: A Review of the Dual Role of Cytokines.Journal of immunology research · 2021Review
- Targeting nuclear acid-mediated immunity in cancer immune checkpoint inhibitor therapies.Signal transduction and targeted therapy · 2020Review
- Caspase-8 mediates inflammation and disease in rodent malaria.Nature communications · 2020Article
- RTP4 inhibits IFN-I response and enhances experimental cerebral malaria and neuropathology.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Differential IL-18 Dependence of Canonical and Adaptive NK Cells for Antibody Dependent Responses toFrontiers in immunology · 2020Article
- Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020Review
- The Roles of Type I Interferon in Co-infections With Parasites and Viruses, Bacteria, or Other Parasites.Frontiers in immunology · 2020Review
- Autophagy in the control and pathogenesis of parasitic infections.Cell & bioscience · 2020Review
- Monocyte-derived dendritic cells in malaria.Current opinion in microbiology · 2019Review
- Human TLR8 Senses RNA FromFrontiers in immunology · 2019Article
- Fetal-Derived MyD88 Signaling Contributes to Poor Pregnancy Outcomes During Gestational Malaria.Frontiers in microbiology · 2019Article
- A malaria protein factor induces IL-4 production by dendritic cells via PI3K-Akt-NF-κB signaling independent of MyD88/TRIF and promotes Th2 response.The Journal of biological chemistry · 2018Article
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Effective resolution of malaria infection by avoiding pathogenesis requires regulated pro- to anti-inflammatory responses and the development of protective immunity. TLRs are known to be critical for initiating innate immune responses, but their roles in the regulation of immune responses and development of protective immunity to malaria remain poorly understood. In this study, using wild-type, TLR2(-/-), TLR4(-/-), TLR9(-/-), and MyD88(-/-) mice infected with Plasmodium yoelii, we show that TLR9 and MyD88 regulate pro/anti-inflammatory cytokines, Th1/Th2 development, and cellular and humoral responses. Dendritic cells from TLR9(-/-) and MyD88(-/-) mice produced significantly lower levels of proinflammatory cytokines and higher levels of anti-inflammatory cytokines than dendritic cells from wild-type mice. NK and CD8(+) T cells from TLR9(-/-) and MyD88(-/-) mice showed markedly impaired cytotoxic activity. Furthermore, mice deficient in TLR9 and MyD88 showed higher Th2-type and lower Th1-type IgGs. Consequently, TLR9(-/-) and MyD88(-/-) mice exhibited compromised ability to control parasitemia and were susceptible to death. Our data also show that TLR9 and MyD88 distinctively regulate immune responses to malaria infection. TLR9(-/-) but not MyD88(-/-) mice produced significant levels of both pro- and anti-inflammatory cytokines, including IL-1β and IL-18, by other TLRs/inflammasome- and/or IL-1R/IL-18R-mediated signaling. Thus, whereas MyD88(-/-) mice completely lacked cell-mediated immunity, TLR9(-/-) mice showed low levels of cell-mediated immunity and were slightly more resistant to malaria infection than MyD88(-/-) mice. Overall, our findings demonstrate that TLR9 and MyD88 play central roles in the immune regulation and development of protective immunity to malaria, and have implications in understanding immune responses to other pathogens.
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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.