ArticleArthritis research & therapy2017
Hydroxychloroquine inhibits CD154 expression in CD4
Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Effects of Hydroxychloroquine on Proteinuria in IgA Nephropathy: A Systematic Review and Meta-Analysis.BioMed research international · 2021Pooled it
- Immunosuppression by hydroxychloroquine: mechanistic proof in in vitro experiments but limited systemic activity in a randomized placebo-controlled clinical pharmacology study.Immunologic research · 2023Trial
- Reduced late endosome/lysosome function promotes SLE through chronic PI3K activity and SHP-1/SHIP-1 defects.JCI insight · 2026Article
- Role of antimalarials in lupus nephritis: a narrative review.Clinical rheumatology · 2025Review
- Lymphocytes Change Their Phenotype and Function in Systemic Lupus Erythematosus and Lupus Nephritis.International journal of molecular sciences · 2024Review
- Trim21-mediated CCT2 ubiquitination suppresses malignant progression and promotes CD4Cell death & disease · 2024Article
- Treatment of Rheumatoid Arthritis Based on the Inherent Bioactivity of Black Phosphorus Nanosheets.Aging and disease · 2024Article
- Network pharmacology-based strategy to investigate the mechanisms of artemisinin in treating primary Sjögren's syndrome.BMC immunology · 2024Article
- Inhibition of CD4 + T cells by fanchinoline via miR506-3p/NFATc1 in Sjögren's syndrome.Inflammopharmacology · 2023Article
- Antimicrobial therapies for chronic pain (part 1): analgesic mechanisms.The Korean journal of pain · 2023Review
- Aberrant B-Cell Activation in Systemic Lupus Erythematosus.Kidney diseases (Basel, Switzerland) · 2022Review
- Hydroxychloroquine induces apoptosis of myeloid-derived suppressor cells via up-regulation of CD81 contributing to alleviate lupus symptoms.Molecular medicine (Cambridge, Mass.) · 2022Article
- The Role of Autophagy in the Function of CD4Frontiers in pharmacology · 2022Review
- Hydroxychloroquine Alleviates EAU by Inhibiting Uveitogenic T Cells and Ameliorating Retinal Vascular Endothelial Cells Dysfunction.Frontiers in immunology · 2022Article
- Disease-duration based comparison of subsets of immune cells in SARS CoV-2 infected patients presenting with mild or severe symptoms identifies prognostic markers for severity.Immunity, inflammation and disease · 2021Article
- Nanocarrier vaccines for SARS-CoV-2.Advanced drug delivery reviews · 2021Article
- Risk management strategies and therapeutic modalities to tackle COVID-19/SARS-CoV-2.Journal of infection and public health · 2021Review
- Insights of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2) pandemic: a current review.Biological procedures online · 2021Review
- The cytokine storm and COVID-19.Journal of medical virology · 2021Review
- Mechanism of Action and Efficacy of Immunosupressors in Lupus Nephritis.International journal of nephrology and renovascular disease · 2021Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOverexpression of membranous CD154 in T lymphocytes has been found previously in systemic lupus erythematosus (SLE). Because hydroxychloroquine (HCQ) has been used frequently in the treatment of lupus, we sought to identify the effects of HCQ on CD154 and a possibly regulatory mechanism.
methodsCD4
resultsHCQ treatment had significant dose-dependent suppressive effects on membranous CD154 expression in ionomycin-activated T cells from lupus patients. Furthermore, HCQ inhibited intracellular sustained calcium storage release, and attenuated the nuclear translocation of NFATc2 and the expression of NFATc1. However, CD154 expressed through IL-15-mediated STAT5 signaling was not inhibited by HCQ treatment.
conclusionsHCQ inhibited NFAT signaling in activated T cells and blocked the expression of membranous CD154, but not STAT5 signaling. These findings provide a mechanistic insight into SLE in HCQ treatment.
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Registered trials
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