ArticleImmunologic research2014
JAK/STAT/PKCδ molecular pathways in synovial fluid T lymphocytes reflect the in vivo T helper-17 expansion in psoriatic arthritis.
Article in Immunologic research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 70 citations in OpenAlex.
- Transcriptomic profiling of secukinumab-treated psoriatic arthritis reveals potential novel response-associated pathways.Rheumatology (Oxford, England) · 2026Observational
- Risk of Major Adverse Cardiovascular Events and Thromboembolism Events in Patients with Psoriatic Arthritis on JAK Inhibitors: A Network Meta-Analysis.Rheumatology and therapy · 2025Review
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
- Drug Target Identification and Drug Repurposing in Psoriasis through Systems Biology Approach, DNN-Based DTI Model and Genome-Wide Microarray Data.International journal of molecular sciences · 2023Article
- JAK Inhibitors in Psoriatic Disease.Clinical, cosmetic and investigational dermatology · 2023Review
- Upadacitinib for the treatment of psoriatic arthritis.Drugs in context · 2023Review
- Article
- Psoriatic arthritis from a mechanistic perspective.Nature reviews. Rheumatology · 2022Review
- Exploring the Diverse Immune and Genetic Landscape of Psoriatic Arthritis.Journal of clinical medicine · 2021Review
- Proteomimetics of Natural Regulators of JAK-STAT Pathway: Novel Therapeutic Perspectives.Frontiers in molecular biosciences · 2021Review
- High Dimensional Analyses of Circulating Immune Cells in Psoriatic Arthritis Detects Elevated Phosphorylated STAT3.Frontiers in immunology · 2021Article
- Targeting JAK-STAT Signalling Alters PsA Synovial Fibroblast Pro-Inflammatory and Metabolic Function.Frontiers in immunology · 2021Article
- Tanshinone IIA and Astragaloside IV Inhibit miR-223/JAK2/STAT1 Signalling Pathway to Alleviate Lipopolysaccharide-Induced Damage in Nucleus Pulposus Cells.Disease markers · 2021Article
- Patient-Centered Care in Psoriatic Arthritis-A Perspective on Inflammation, Disease Activity, and Psychosocial Factors.Journal of clinical medicine · 2020Review
- A novel treatment for psoriatic arthritis: Janus kinase inhibitors.Chinese medical journal · 2020Review
- Experimental and Investigational Pharmacotherapy for Psoriatic Arthritis: Drugs of the Future.Journal of experimental pharmacology · 2020Review
- A specific small-molecule inhibitor of protein kinase CδI activity improves metabolic dysfunction in human adipocytes from obese individuals.The Journal of biological chemistry · 2019Article
- Late-Onset and Elderly Psoriatic Arthritis: Clinical Aspects and Management.Drugs & aging · 2019Review
- Psoriatic disease treatment nowadays: unmet needs among the "jungle of biologic drugs and small molecules".Clinical rheumatology · 2018Article
- Switching Between Biological Treatments in Psoriatic Arthritis: A Review of the Evidence.Drugs in R&D · 2017Review
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Looking to the sustained psoriatic arthritis (PsA) joint as a model of local human inflammation, this study was designed to assess the T lymphocyte signal transduction pathways potentially involved in this chronic immune-mediated inflammatory process, as characterized by direct ex vivo analysis of T helper (Th)-17 T effector (Teff) cell phenotypes in synovial fluid (SF) and peripheral blood (PB) of clinically active PsA patients. The reverse-phase protein arrays (RPPA) technique was employed to identify STAT3, STAT1, JAK1, JAK2, PKCδ and ERK1/2 phosphoprotein levels on total T cell lysates in SF samples of PsA patients. Frequencies of T CD4(+)IL-17A-F(+) and T CD4(+)IL-23R(+) Th17 cells were quantified in SF and matched PB of PsA patients by flow cytometry and compared with PB of healthy controls (HC). Increased levels of JAK1, STAT3, STAT1 and PKCδ phosphoproteins were found in SF T cells of PsA patients, compared with PB of HC. The expansion of T CD4(+)IL-17A-F(+) cells, as well as of T CD4(+) cells expressing IL-23Rp19 (T CD4(+) IL-23R(+)), considered as the pathogenic phenotype of effector Th17 cells, was found to be confined to the joints of PsA patients, as the frequencies of both populations were significantly higher in SF than in matched PB, or in PB of HC. In conclusion, T lymphocyte signal transduction pathway mapping revealed an enhanced activation of JAK1/STAT3/STAT1 and PKCδ phosphoproteins that may drive the local inflammatory process, characterized by the in vivo expansion of T CD4(+)IL-17A-F(+) and T CD4(+)IL-23R(+) Th17 Teff cells in SF of clinically active joints of PsA patients.
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