ArticleProceedings of the National Academy of Sciences of the United States of America2013
MyD88 is essential to sustain mTOR activation necessary to promote T helper 17 cell proliferation by linking IL-1 and IL-23 signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 87 citations in OpenAlex.
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- Perspective: Personalized Management of Oxidative and Nitrosative Stress in Post-Exercise Recovery with a Particular Emphasis on the Potential of Micro-Immunotherapy.Sports (Basel, Switzerland) · 2026Review
- MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.Immunology · 2026Article
- Leishmania amazonensis infection induces PD-L1 expression on dendritic cells and impairs Th1 responses in vitro and in vivo.Scientific reports · 2025Article
- Hyperresponsiveness of Corticoid-Resistant Th17/Tc-17 Cells to TLR-2 and TLR-4 Ligands is a Feature of Multiple Sclerosis Patients at Higher Risk of Therapy Failure.Journal of inflammation research · 2024Article
- Signaling Pathways Leading to mTOR Activation Downstream Cytokine Receptors in Lymphocytes in Health and Disease.International journal of molecular sciences · 2023Review
- Classic costimulatory interactions in MAIT cell responses: from gene expression to immune regulation.Clinical and experimental immunology · 2023Article
- GSDMD in peripheral myeloid cells regulates microglial immune training and neuroinflammation in Parkinson's disease.Acta pharmaceutica Sinica. B · 2023Article
- Key Genes of Immunity Associated with Pterygium and Primary Sjögren's Syndrome.International journal of molecular sciences · 2023Article
- Factors impacting the benefits and pathogenicity of Th17 cells in the tumor microenvironment.Frontiers in immunology · 2023Review
- TH17 cells promote CNS inflammation by sensing danger signals via Mincle.Nature communications · 2022Article
- Toll-Like Receptor Signaling and Its Role in Cell-Mediated Immunity.Frontiers in immunology · 2022Review
- The Th1/Tfh-like biased responses elicited by the rASP-1 innate adjuvant are dependent on TRIF and Type I IFN receptor pathways.Frontiers in immunology · 2022Article
- Pseudomonas aeruginosa outer membrane vesicles ameliorates lung ischemia-reperfusion injury by regulating the balance of regulatory T cells and Th17 cells through Tim-3 and TLR4/NF-κB pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Differential controls of MAIT cell effector polarization by mTORC1/mTORC2 via integrating cytokine and costimulatory signals.Nature communications · 2021Article
- Control of T Cell Metabolism by Cytokines and Hormones.Frontiers in immunology · 2021Review
- Review
- mTOR signaling at the crossroads of environmental signals and T-cell fate decisions.Immunological reviews · 2020Review
- Pharmacological Activation of Pyruvate Kinase M2 Inhibits CD4Cell metabolism · 2020Article
- Interleukin-1 as Innate Mediator of T Cell Immunity.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Myeloid differentiation primary response protein 88 (MyD88) is classically known as an adaptor, linking TLR and IL-1R to downstream signaling pathways in the innate immune system. In addition to its role in innate immune cells, MyD88 has been shown to play an important role in T cells. How MyD88 regulates helper T-cell differentiation remains largely unknown, however. Here we demonstrate that MyD88 is an important regulator of IL-17-producing CD4(+) T helper cells (Th17) cell proliferation. MyD88-deficient CD4(+) T cells showed a defect in Th17 cell differentiation, but not in Th1 cell or Th2 cell differentiation. The impaired IL-17 production from MyD88-deficient CD4(+) T cells is not a result of defective RAR-related orphan receptor γt (RORγt) expression. Instead, MyD88 is essential for sustaining the mammalian target of rapamycin (mTOR) activation necessary to promote Th17 cell proliferation by linking IL-1 and IL-23 signaling. MyD88-deficient CD4(+) T cells showed impaired mTOR activation and, consequently, reduced Th17 cell proliferation. Importantly, the absence of MyD88 in T cells ameliorated disease in the experimental autoimmune encephalomyelitis model. Taken together, our results demonstrate that MyD88 has a dual function in Th17 cells by delivering IL-1 signaling during the early differentiation stage and integrating IL-23 signaling to the mTOR complex to expand committed Th17 cells.
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