ArticleJournal of immunology (Baltimore, Md. : 1950)2018
Reciprocal Regulation of Glycolysis-Driven Th17 Pathogenicity and Regulatory T Cell Stability by Cdc42.
Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 45 citations in OpenAlex.
- Implications of Rho GTPase signaling in cancer immunotherapy.Biochemical Society transactions · 2026Review
- Glucose metabolic reprogramming in systemic lupus erythematosus and lupus nephritis: theoretical foundations and therapeutic implications.Frontiers in immunology · 2026Review
- Genetic and epigenetic regulation of Treg cell fitness by autism-related chromatin remodeler CHD8.Cellular & molecular biology letters · 2025Article
- Systemic lupus erythematosus: updated insights on the pathogenesis, diagnosis, prevention and therapeutics.Signal transduction and targeted therapy · 2025Review
- CDC42 Regulatory Patterns Related To Inflammatory Bowel Disease and Hyperglycemia.Journal of bioinformatics and systems biology : Open access · 2025Article
- Review
- Unveiling shared therapeutic targets and pathological pathways between coronary artery disease and major depressive disorder through bioinformatics analysis.Scientific reports · 2024Article
- DIAPH1-Deficiency is Associated with Major T, NK and ILC Defects in Humans.Journal of clinical immunology · 2024Article
- Correlation of the serum cell division cycle 42 with CD4Frontiers in cardiovascular medicine · 2024Article
- Pathways and molecules for overcoming immunotolerance in metastatic gastrointestinal tumors.Frontiers in immunology · 2024Review
- The clinical utility of circulating cell division control 42 in small-vessel coronary artery disease patients undergoing drug-coated balloon treatment.BMC cardiovascular disorders · 2023Article
- Role of Rho GTPases in inflammatory bowel disease.Cell death discovery · 2023Review
- Linkage of blood cell division cycle 42 with T helper cells, and their correlation with anxiety, depression, and cognitive impairment in stroke patients.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- Cell division control protein 42 correlates with lower disease risk and its elevation predicts better treatment response, and inhibits T-helper 17 cell differentiation in rheumatoid arthritis.Inflammopharmacology · 2022Article
- Targeting of Cdc42 GTPase in regulatory T cells unleashes antitumor T-cell immunity.Journal for immunotherapy of cancer · 2022Article
- The relationship of blood CDC42 level with Th1 cells, Th17 cells, inflammation markers, disease risk/activity, and treatment efficacy of rheumatoid arthritis.Irish journal of medical science · 2022Article
- The relation of circulating cell division cycle 42 expression with Th1, Th2, and Th17 cells, adhesion molecules, and biochemical indexes in coronary heart disease patients.Irish journal of medical science · 2022Article
- Relation of CDC42, Th1, Th2, and Th17 cells with cognitive function decline in Alzheimer's disease.Annals of clinical and translational neurology · 2022Article
- Blood CDC42 overexpression is associated with an increased risk of acute exacerbation, inflammation and disease severity in patients with chronic obstructive pulmonary disease.Experimental and therapeutic medicine · 2022Article
- Aberrant blood cell division cycle 42 expression and its correlation with disease severity, inflammation and mortality risk in patients with acute pancreatitis.Experimental and therapeutic medicine · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
A balance between Th17 cells and regulatory T cells (Tregs) is important for host immunity and immune tolerance. The underlying molecular mechanisms remain poorly understood. Here we have identified Cdc42 as a central regulator of Th17/Treg balance. Deletion of Cdc42 in T cells enhanced Th17 differentiation but diminished induced Treg differentiation and suppressive function. Treg-specific deletion of Cdc42 decreased natural Tregs but increased effector T cells including Th17 cells. Notably, Cdc42-deficient Th17 cells became pathogenic associated with enhanced glycolysis and Cdc42-deficient Tregs became unstable associated with weakened glycolytic signaling. Inhibition of glycolysis in Cdc42-deficient Th17 cells diminished their pathogenicity and restoration of glycolysis in Cdc42-deficient Tregs rescued their instability. Intriguingly, Cdc42 deficiency in T cells led to exacerbated wasting disease in mouse models of colitis and Treg-specific deletion of Cdc42 caused early, fatal lymphoproliferative diseases. In summary, we show that Cdc42 is a bona fide regulator of peripheral tolerance through suppression of Th17 aberrant differentiation/pathogenicity and promotion of Treg differentiation/stability/function involving metabolic signaling and thus Cdc42 pathway might be harnessed in autoimmune disease therapy.
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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.