ArticleEMBO reports2019
STAT3 but not STAT4 is critical for γδT17 cell responses and skin inflammation.
Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- NLRP3-inflammasome Related Genes as Emerging Biomarkers and Therapeutic Targets in Psoriasis.Inflammation · 2025Article
- An Immunomodulating Peptide with Potential to Promote Anticancer Immunity Without Compromising Immune Tolerance.Biomedicines · 2025Article
- Restriction of innate Tγδ17 cell plasticity by an AP-1 regulatory axis.Nature immunology · 2025Article
- IL-17 A expression negatively correlates with γδ T-Cell density in human psoriasis lesions: a novel implication for disease pathogenesis.BMC immunology · 2025Article
- Niclosamide Alleviated Skin Inflammation and Restored the Balance between Effector and Regulatory T Cells in Skin.Biomolecules & therapeutics · 2025Article
- Targeting the STAT3/IL-36G signaling pathway can be a promising approach to treat rosacea.Journal of advanced research · 2025Article
- Metabolic reprogramming of interleukin-17-producing γδ T cells promotes ACC1-mediated de novo lipogenesis under psoriatic conditions.Nature metabolism · 2025Article
- Differential Regulation of Immune-Related Genes in the Developing Heart.Pediatric cardiology · 2025Article
- Indoleamine 2,3-dioxygenase-galectin-3 fusion protein remodels inflammatory and fibrotic programs, ameliorating imiquimod-induced psoriasis.npj biomedical innovations · 2025Article
- Uncovering the mysteries of human gamma delta T cells: from origins to novel therapeutics.Frontiers in immunology · 2025Review
- Restriction of innate Tγδ17 cell plasticity by an AP-1 regulatory axis.bioRxiv : the preprint server for biology · 2024Article
- Visible light accelerates skin wound healing and alleviates scar formation in mice by adjusting STAT3 signaling.Communications biology · 2024Article
- The oncogenic kinase TOPK upregulates in psoriatic keratinocytes and contributes to psoriasis progression by regulating neutrophils infiltration.Cell communication and signaling : CCS · 2024Article
- IL-27 disturbs lipid metabolism and restrains mitochondrial activity to inhibit γδ T17 cell-mediated skin inflammation.Cell death & disease · 2024Article
- Intermittent fasting alleviates IMQ-induced psoriasis-like dermatitis via reduced γδT17 and monocytes in mice.Archives of dermatological research · 2024Article
- STAT3 and SOX-5 induce BRG1-mediated chromatin remodeling of RORCE2 in Th17 cells.Communications biology · 2024Article
- The cIAP ubiquitin ligases sustain type 3 γδ T cells and ILC during aging to promote barrier immunity.The Journal of experimental medicine · 2023Article
- Blood transcriptome analysis suggests an indirect molecular association of early life adversities and adult social anxiety disorder by immune-related signal transduction.Frontiers in psychiatry · 2023Article
- Integrated bioinformatics and machine learning algorithms reveal the critical cellular senescence-associated genes and immune infiltration in heart failure due to ischemic cardiomyopathy.Frontiers in immunology · 2023Article
- Norcantharidin ameliorates the development of murine lupus via inhibiting the generation of IL-17 producing cells.Acta pharmacologica Sinica · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factors STAT3 and STAT4 are essential for lymphocyte differentiation and function. Interleukin (IL)-17 producing γδ T (γδT17) cells are innate lymphocytes important for anti-bacterial and inflammatory responses at barrier surfaces. Herein, we examine the role of STAT3 and STAT4 in regulating the homeostasis, activation, and pathogenicity of γδT17 cells. We show that STAT3 sustains γδT17 numbers in the skin but not in the lymph nodes, while STAT4 deficiency does not affect their homeostasis. Similarly, STAT3 but not STAT4 is essential for IL-23-induced IL-22 production by γδT17 cells. Concomitantly, mice lacking STAT3 expression in γδT17 cells develop significantly reduced psoriasis-like inflammation. STAT3-deficient γδT17 cells fail to expand and to upregulate IL-17A, IL-17F, and IL-22 in response to psoriatic stimuli. Although STAT4-deficient animals develop psoriasis-like disease, γδT17 cells in these mice are defective in IL-17F production. Collectively, our data demonstrate for the first time a critical role for STAT3 in orchestrating the homeostasis and pathogenicity of γδT17 cells and provide evidence for the requirement of STAT4 for optimal cytokine responses during inflammation.
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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.