ArticleJournal of immunology research2015
IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2.
Article in Journal of immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Role of IL-34 in Tumors and Its Application to Regulate Inflammation.Cancer science · 2025Review
- IL-34 aggravates myocardial ischemia-reperfusion injury by upregulating the HMGB1-IL-17A-IL-6 axis through the JAK signaling pathway.PloS one · 2025Article
- Inflammatory cytokine signalling in vulvovaginal candidiasis: a hot mess driving immunopathology.Oxford open immunology · 2024Review
- Interleukin-34 permits Porphyromonas gingivalis survival and NF-κB p65 inhibition in macrophages.Molecular oral microbiology · 2022Article
- LncRNA: A Potential Target for Host-Directed Therapy ofPharmaceutics · 2022Review
- The molecular features of normal and atopic dermatitis skin in infants, children, adolescents, and adults.The Journal of allergy and clinical immunology · 2021Article
- Hippophae rhamnoides mediate gene expression profiles against keratinocytes infection of Staphylococcus aureus.Molecular biology reports · 2021Article
- Immunomodulation of Interleukin-34 and its Potential Significance as a Disease Biomarker and Therapeutic Target.International journal of biological sciences · 2019Review
- Interleukin-34 Regulates Th1 and Th17 Cytokine Production by Activating Multiple Signaling Pathways through CSF-1R in Chicken Cell Lines.International journal of molecular sciences · 2018Article
- Differential Behavior of Non-Frontiers in microbiology · 2018Article
- Immunoregulatory properties of the cytokine IL-34.Cellular and molecular life sciences : CMLS · 2017Review
- Dectin-1 is required for miR155 upregulation in murine macrophages in response to Candida albicans.Virulence · 2017Article
- Functions of interleukin-34 and its emerging association with rheumatoid arthritis.Immunology · 2016Review
- [Progress on the role of Toll-like receptors in Candida albicans infections].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2016Article
- Epithelial responses and Candida albicans pathogenicity are enhanced in the presence of oral streptococci.Brazilian dental journalArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida albicans is a fungus that is an opportunistic pathogen of humans. Normally, C. albicans exists as a harmless commensal and does not trigger inflammatory responses by resident macrophages in skin mucosa, which may be caused by a tolerance of skin macrophage to C. albicans. IL-34 is a recently discovered cytokine, constitutively expressed by keratinocytes in the skin. IL-34 binds to the receptor of M-CSF, thereby stimulating tissue macrophage maturation and differentiation. Resident macrophages exhibit phenotypic plasticity and may transform into inflammatory M1 macrophages for immunity or anti-inflammatory M2 macrophages for tissue repair. M1 macrophages produce higher levels of inflammatory cytokines such as TNFα in response to C. albicans stimulation. In this study, it was demonstrated that IL-34 attenuated TNFα production by M1 macrophages challenged with heat killed Candida (HKC). The molecular mechanism of IL-34 mediated suppression of HKC induced TNFα production by M1 macrophages was by the inhibition of M1 macrophage expression of key C. albicans pattern recognition receptors (PPRs), namely, Toll-like receptor (TLR) 2 and Dectin-1. The results of this study indicated that constitutive IL-34 expressed by skin keratinocytes might suppress resident macrophage responses to C. albicans colonisation by maintaining low levels TLR2 and Dectin-1 expression by macrophages.
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Registered trials
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