ArticlePloS one2014
Protein kinase C θ regulates the phenotype of murine CD4+ Th17 cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Protein Kinase C Family: Structures, Biological Functions, Diseases, and Pharmaceutical Interventions.MedComm · 2025Review
- Proteome characterization of extracellular vesicles from human milk: Uncovering the surfaceome by a lipid-based protein immobilization technology.Journal of extracellular biology · 2024Article
- Review
- Addressing the role of PKD3 in the T cell compartment with knockout mice.Cell communication and signaling : CCS · 2022Article
- Signal Transduction in Immune Cells and Protein Kinases.Advances in experimental medicine and biology · 2021Article
- AEB-071 Ameliorates Muscle Weakness by Altering Helper T Lymphocytes in an Experimental Autoimmune Myasthenia Gravis Rat Model.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Novel mutant mouse line emphasizes the importance of protein kinase C theta for CD4Cell communication and signaling : CCS · 2019Article
- Pharmacological Inhibition of PKCθ Counteracts Muscle Disease in a Mouse Model of Duchenne Muscular Dystrophy.EBioMedicine · 2017Article
- Protein kinase C theta is dispensable for suppression mediated by CD25+CD4+ regulatory T cells.PloS one · 2017Article
- Interleukin-15 promotes intestinal dysbiosis with butyrate deficiency associated with increased susceptibility to colitis.The ISME journal · 2017Article
- Proof of Principle for a T Lymphocyte Intrinsic Function of Coronin 1A.The Journal of biological chemistry · 2016Article
- Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Protein kinase C θ (PKCθ) is involved in signaling downstream of the T cell antigen receptor (TCR) and is important for shaping effector T cell functions and inflammatory disease development. Acquisition of Th1-like effector features by Th17 cells has been linked to increased pathogenic potential. However, the molecular mechanisms underlying Th17/Th1 phenotypic instability remain largely unknown. In the current study, we address the role of PKCθ in differentiation and function of Th17 cells by using genetic knock-out mice. Implementing in vitro (polarizing T cell cultures) and in vivo (experimental autoimmune encephalomyelitis model, EAE) techniques, we demonstrated that PKCθ-deficient CD4+ T cells show normal Th17 marker gene expression (interleukin 17A/F, RORγt), accompanied by enhanced production of the Th1-typical markers such as interferon gamma (IFN-γ) and transcription factor T-bet. Mechanistically, this phenotype was linked to aberrantly elevated Stat4 mRNA levels in PKCθ-/- CD4+ T cells during the priming phase of Th17 differentiation. In contrast, transcription of the Stat4 gene was suppressed in Th17-primed wild-type cells. This change in cellular effector phenotype was reflected in vivo by prolonged neurological impairment of PKCθ-deficient mice during the course of EAE. Taken together, our data provide genetic evidence that PKCθ is critical for stabilizing Th17 cell phenotype by selective suppression of the STAT4/IFN-γ/T-bet axis at the onset of differentiation.
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