ArticleArthritis & rheumatology (Hoboken, N.J.)2016
Calcium/Calmodulin-Dependent Kinase IV Facilitates the Recruitment of Interleukin-17-Producing Cells to Target Organs Through the CCR6/CCL20 Axis in Th17 Cell-Driven Inflammatory Diseases.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Macrophage-derived CCL20 promotes abdominal aortic aneurysm progression via lymphocytes CCR6.Frontiers in immunology · 2026Article
- Identification of differentially expressed immune-related genes in patients with systemic lupus erythematosus and the development of a hub gene-based diagnostic model.European journal of medical research · 2025Article
- ZDHHC14-Mediated TEAD4 Palmitoylation Drives Th17 Cell Recruitment in Renal Immunopathology.Research (Washington, D.C.) · 2025Article
- Progress of CCL20-CCR6 in the airways: a promising new therapeutic target.Journal of inflammation (London, England) · 2024Review
- Exosomes secreted by podocytes regulate the differentiation of Th17/Treg cells in idiopathic nephrotic syndrome.Heliyon · 2024Article
- CaMK4 controls follicular helper T cell expansion and function during normal and autoimmune T-dependent B cell responses.Nature communications · 2024Article
- Altered Circulating Follicular T Helper Cell Subsets and Follicular T Regulatory Cells Are Indicators of a Derailed B Cell Response in Lupus, Which Could Be Modified by Targeting IL-21R.International journal of molecular sciences · 2022Article
- IFN-γ, should not be ignored in SLE.Frontiers in immunology · 2022Review
- A Mechanistic Insight into the Pathogenic Role of Interleukin 17A in Systemic Autoimmune Diseases.Mediators of inflammation · 2022Review
- Altered circulating CCR6Arthritis research & therapy · 2021Article
- Effect of interleukin-6, -17, -21, -22, and -23 and STAT3 on signal transduction pathways and their inhibition in autoimmune arthritis.Immunologic research · 2021Review
- A Functional Variant rs3093023 inFrontiers in immunology · 2021Article
- Mesenchymal Stem Cell Protects Injured Renal Tubular Epithelial Cells by Regulating mTOR-Mediated Th17/Treg Axis.Frontiers in immunology · 2021Review
- The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis.Frontiers in medicine · 2021Review
- Calcium/calmodulin-dependent protein kinase IV signaling pathway is upregulated in experimental necrotizing enterocolitis.Pediatric surgery international · 2020Article
- Current Insights and Future Prospects for Targeting IL-17 to Treat Patients With Systemic Lupus Erythematosus.Frontiers in immunology · 2020Review
- Dysregulated T Cell Activation and Aberrant Cytokine Expression Profile in Systemic Lupus Erythematosus.Mediators of inflammation · 2019Article
- Emerging areas for therapeutic discovery in SLE.Current opinion in immunology · 2018Review
- CCR6PeerJ · 2018Article
- Expression of CCR6 in esophageal squamous cell carcinoma and its effects on epithelial-to-mesenchymal transition.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveThe recruitment of interleukin-17 (IL-17)-producing T helper (Th17) cells to inflammatory sites has been implicated in the development of organ damage in inflammatory and autoimmune diseases including systemic lupus erythematosus (SLE). To define the mechanism of calcium/calmodulin-dependent kinase IV (CaMKIV) activation of Th17 cell recruitment to target tissues, we performed anti-glomerular basement membrane antibody-induced glomerulonephritis (AIGN) experiments in mice and studied samples from patients with SLE.
methodsWe induced experimental AIGN in CaMKIV-sufficient or CaMKIV-deficient mice and compared histology, Th17 cell-related chemokine expression, and numbers of IL-17-producing cells in kidneys. We also evaluated the efficacy of the CaMKIV inhibitor KN-93 in AIGN-induced kidney disease. The expression of CCR6 in memory CD4+ T cells before AIGN induction was analyzed by flow cytometry. We investigated the correlation between CCR6 expression in peripheral blood and the severity of glomerulonephritis in patients with SLE.
resultsCaMKIV-deficient mice displayed less glomerular injury after induction of AIGN. Kidney infiltration by IL-17-producing CD4+ T cells along with CCR6 and CCL20 expression were significantly decreased in CaMKIV-deficient mice. Similarly, treatment of mice with KN-93 improved clinical and pathologic outcomes. Expression and function of CCR6 in peripheral blood memory CD4+ T cells was decreased in CaMKIV-deficient mice. Expression of CCR6 correlated positively with severity of organ damage in SLE patients.
conclusionCaMKIV inhibition represents a novel therapeutic strategy for treatment of Th17 cell-mediated tissue damage in inflammatory diseases.
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