ArticleJournal of leukocyte biology2020
Calcineurin inhibitors reduce NFAT-dependent expression of antifungal pentraxin-3 by human monocytes.
Article in Journal of leukocyte biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- TRP120-dependent activation of noncanonical Wnt/NFAT signaling drives monocyte chemokine production inmSphere · 2026Article
- Calcineurin/NFAT signaling in the temporal integration of Ca²⁺ stress in neurodegeneration.Cell death discovery · 2026Review
- MCP1 Inverts the Correlation between FGF23 and Omega 6/3 Ratio: Is It Also True in Renal Transplantation?Journal of clinical medicine · 2023Article
- Nuclear factor of activated T-cells (NFAT) regulation of IL-1β-induced retinal vascular inflammation.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- NFAT signaling in human mesenchymal stromal cells affects extracellular matrix remodeling and antifungal immune responses.iScience · 2021Article
- NFAM1 Promotes Pro-Inflammatory Cytokine Production in Mouse and Human Monocytes.Frontiers in immunology · 2021Article
- Immunosuppression Affects Neutrophil Functions: Does Calcineurin-NFAT Signaling Matter?Frontiers in immunology · 2021Review
- Roles of IL-2 in bridging adaptive and innate immunity, and as a tool for cellular immunotherapy.Journal of leukocyte biology · 2020Review
- Calcineurin inhibitors reduce NFAT-dependent expression of antifungal pentraxin-3 by human monocytes.Journal of leukocyte biology · 2020Article
- Cellular and molecular mechanisms of antifungal innate immunity at epithelial barriers: The role of C-type lectin receptors.European journal of immunology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcineurin (CN) inhibitors are effective clinical immunosuppressants but leave patients vulnerable to potentially fatal fungal infections. This study tested the hypothesis that CN inhibition interferes with antifungal immune defenses mediated by monocytes. We showed that NFAT is expressed by human monocytes, and is activated by exposure to fungal ligands. We confirmed that NFAT translocation potently activated target gene transcription using a human monocytic reporter cell line. Inhibition of CN-NFAT by cyclosporine A significantly reduced monocyte production of TNF-α, IL-10, and MCP-1 proteins in response to pattern recognition receptor ligands as well as to Aspergillus fumigatus conidia. Moreover, we revealed that human monocytes express the antifungal protein pentraxin-3 under control of NFAT. In conclusion, clinical CN inhibitors have the potential to interfere with the novel NFAT-dependent pentraxin-3 pathway as well as antifungal cytokine production in human monocytes, thereby impeding monocyte-mediated defenses against fungal infection in immune-suppressed patients.
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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.