ArticleProceedings of the National Academy of Sciences of the United States of America2008
T cell expression of MyD88 is required for resistance to Toxoplasma gondii.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 109 citations in OpenAlex.
- MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.Immunology · 2026Article
- The structure and functions of TRAF families and recent advances of TRAFs in leukemia.Frontiers in oncology · 2026Review
- A new immunological paradigm for diseases: the protein-homeostasis-system hypothesis.Frontiers in immunology · 2026Review
- Review
- IL-24 Is a Promising Molecular Adjuvant for Enhancing Protective Immunity Induced by DNA Vaccination AgainstMicroorganisms · 2025Article
- Influence of MyD88 and αβ T cells on mesenteric lymph node innate lymphoid cell populations during Toxoplasma gondii infection.PloS one · 2025Article
- IL-36 Gamma: A Novel Adjuvant Cytokine Enhancing Protective Immunity Induced by DNA Immunization with TGIST and TGNSM AgainstMicroorganisms · 2024Article
- Immunogenicity of lipid nanoparticles and its impact on the efficacy of mRNA vaccines and therapeutics.Experimental & molecular medicine · 2023Review
- Co-Immunization with DNA Vaccines Expressing SABP1 and SAG1 Proteins Effectively Enhanced Mice Resistance toVaccines · 2023Article
- Myeloid MyD88 restricts CD8Scientific reports · 2023Article
- IL-18BP mediates the balance between protective and pathological immune responses to Toxoplasma gondii.Cell reports · 2023Article
- Impact of MyD88, Microbiota, and Location on Type 1 and Type 3 Innate Lymphoid Cells duringImmunoHorizons · 2022Article
- Cytotoxic CD4eLife · 2022Article
- Review
- Induction of IL-12p40 and type 1 immunity by Toxoplasma gondii in the absence of the TLR-MyD88 signaling cascade.PLoS pathogens · 2021Article
- The role of IL-12 in stimulating NK cells against Toxoplasma gondii infection: a mini-review.Parasitology research · 2021Review
- IL-33 promotes innate lymphoid cell-dependent IFN-γ production required for innate immunity toeLife · 2021Article
- MAP3K2 augments Th1 cell differentiation via IL-18 to promote T cell-mediated colitis.Science China. Life sciences · 2021Article
- Immunization With a DNA Vaccine Encoding theFrontiers in microbiology · 2021Article
- Protective Immunity Induced by TgMIC5 and TgMIC16 DNA Vaccines Against Toxoplasmosis.Frontiers in cellular and infection microbiology · 2021Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Resistance to Toxoplasma gondii depends on dendritic cells to recognize this pathogen and secrete IL-12, in turn promoting IFN-gamma production from responding T cells. The adaptor protein, myeloid differentiation primary-response gene 88 (MyD88), is important for most Toll-like receptor (TLR) signaling, as well as IL-1R/IL-18R signals. There is considerable evidence that MyD88 is required for the innate sensing of T. gondii and IL-12 responses. Although Myd88(-/-) mice challenged with T. gondii have defective IL-12 and Th1 effector responses and succumb to disease, administration of IL-12 to Myd88(-/-) mice partially restores the Th1 response and yet fails to prolong survival. This finding suggested that MyD88 may mediate signals within T cells important for resistance to this pathogen. To evaluate the role of MyD88 in T cells under noncompetitive conditions, bone marrow chimeras were generated, in which the T cells lacked MyD88, but MyD88-dependent innate immune responses were intact. Upon challenge with T. gondii, these chimeric mice were more susceptible to disease, developing severe toxoplasmic encephalitis and succumbing within 30 days. Splenocytes and brain mononuclear cells isolated from infected chimeric mice produced less IFN-gamma when cultured with a T. gondii-derived antigen. The increase in susceptibility observed was independent of signals via the IL-1R and IL-18R, suggesting a role for TLRs in MyD88-mediated T cell responses to T. gondii. These observations show that, in addition to a role for MyD88 in innate responses, T cell expression of MyD88 is necessary for prolonged resistance to a pathogen.
Indexed as
Identifiers
What OpenQuestion holds
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.