The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Up-regulated expression of CD86 on circulating intermediate monocytes correlated with disease severity in psoriasis
Abstract
Background The number of intermediate monocytes (CD14 ++ CD16 + ) increases in many inflammatory conditions. However, it is not yet known which functional markers expressed by these populations are linked to the pathogenesis of psoriasis. Objectives We evaluated the expression of functional markers on circulating intermediate monocytes. Our goal was to correlate specific populations and their markers with the clinical severity of psoriasis. Methods A cohort of 43 psoriatic patients was subjected to analysis. The proportion of intermediate monocytes with CD86 expression was evaluated by flow cytometry. Serum beta defensin-2 levels were measured by ELISA. Immunofluorescent staining was performed in order to identify the presence of CD14 + CD16 + cells that co-expressed CD86 in affected skin tissues. Results Upregulated expression of CD86 on the intermediate subset (but not the number of intermediate monocytes) correlated with clinical severity as measured by PASI scores and serum beta defensin-2 levels. Immunostaining also showed the presence of CD86 + CD14 + CD16 + cells in the epidermis and dermis of psoriatic plaques, which was associated with increased epidermal proliferation. Conclusion These results suggest that the expression of CD86 on circulating intermediate monocytes could be used as an index in clinical practice and provide novel insights into how these cells join a complex immune network under the pathological conditions of psoriasis.
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“psoriasis is characterized by increased frequencies of M1-like monocytes in the peripheral blood and enhanced infiltration of M1 macrophages within lesional skin18–21.”
From Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis (2026) · cites this paper as [19]
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Miele, L., Vallone, S., Cefalo, C., La Torre, G., Di Stasi, C., Vecchio, F. M., D’Agostino, M., Gabrieli, M. L., Vero, V., Biolato, M., et al. (2009) · Journal of Hepatology · doi:10.1016/j.jhep.2009.06.008 · Cited by 249
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Research works printed but not linked: 26
- Zawada, 2011, SuperSAGE evidence for CD14++CD16+ monocytes as a third monocyte subset, Blood, 118, e50, 10.1182/blood-2011-01-326827 · DOI
- Wong, 2011, Gene expression profiling reveals the defining features of the classical, intermediate, and nonclassical human monocyte subsets, Blood, 118, e16, 10.1182/blood-2010-12-326355 · DOI
- Belge, 2002, The proinflammatory CD14+CD16+DR++ monocytes are a major source of TNF, J. Immunol., 168, 3536, 10.4049/jimmunol.168.7.3536 · DOI
- Frankenberger, 1996, Differential cytokine expression in human blood monocyte subpopulations: a polymerase chain reaction analysis, Blood, 87, 373, 10.1182/blood.V87.1.373.373 · DOI
- Wong, 2012, The three human monocyte subsets: implications for health and disease, Immunol. Res., 53, 41, 10.1007/s12026-012-8297-3 · DOI
- Golden, 2015, Chronic psoriatic skin inflammation leads to increased monocyte adhesion and aggregation, J. Immunol., 195, 2006, 10.4049/jimmunol.1402307 · DOI
- Fujisawa, 2012, Adsorptive depletion of CD14(+)CD16(+) proinflammatory monocyte phenotype in patients with generalized pustular psoriasis: clinical efficacy and effects on cytokines, Ther. Apher. Dial., 16, 436, 10.1111/j.1744-9987.2012.01108.x · DOI
- Yamanaka, 2014, Biologic therapy improves psoriasis by decreasing the activity of monocytes and neutrophils, J. Dermatol., 41, 679, 10.1111/1346-8138.12560 · DOI
- Augustin, 2017, Incremental burden of cardiovascular comorbidity and psoriatic arthritis among adults with moderate-to-severe psoriasis in five European countries, J. Eur. Acad. Dermatol. Venereol., 31, 1316, 10.1111/jdv.14286 · DOI
- Imhof, 2004, Adhesion mechanisms regulating the migration of monocytes, Nat. Rev. Immunol., 4, 432, 10.1038/nri1375 · DOI
- Pai, 2006, Polymorphisms in the CC-chemokine receptor-2 (CCR2) and -5 (CCR5) genes and risk of coronary heart disease among US women, Atherosclerosis, 186, 132, 10.1016/j.atherosclerosis.2005.06.041 · DOI
- Rogacev, 2011, CD14++CD16+ monocytes and cardiovascular outcome in patients with chronic kidney disease, Eur. Heart J., 32, 84, 10.1093/eurheartj/ehq371 · DOI
- Tonel, 2010, Cutting edge: a critical functional role for IL-23 in psoriasis, J. Immunol., 185, 5688, 10.4049/jimmunol.1001538 · DOI
- Mitra, 1995, Psoriatic skin-derived dendritic cell function is inhibited by exogenous IL-10. Differential modulation of B7-1 (CD80) and B7-2 (CD86) expression, J. Immunol., 154, 2668, 10.4049/jimmunol.154.6.2668 · DOI
- Johansen, 2016, Characterization of TNF-alpha- and IL-17A-mediated synergistic induction of DEFB4 gene expression in human keratinocytes through IkappaBzeta, J. Invest. Dermatol., 136, 1608, 10.1016/j.jid.2016.04.012 · DOI
- Kolbinger, 2017, beta-Defensin 2 is a responsive biomarker of IL-17A-driven skin pathology in patients with psoriasis, J. Allergy Clin. Immunol., 139, 923, 10.1016/j.jaci.2016.06.038 · DOI
- Rohrl, 2010, Human beta-defensin 2 and 3 and their mouse orthologs induce chemotaxis through interaction with CCR2, J. Immunol., 184, 6688, 10.4049/jimmunol.0903984 · DOI
- Jansen, 2009, Beta-defensin-2 protein is a serum biomarker for disease activity in psoriasis and reaches biologically relevant concentrations in lesional skin, PLoS One, 4, e4725, 10.1371/journal.pone.0004725 · DOI
- Perera, 2012, Psoriasis, Annu. Rev. Pathol., 7, 385, 10.1146/annurev-pathol-011811-132448 · DOI
- Finet, 2016, Liver test abnormalities in patients admitted for severe psoriasis: prevalence and associated risk factors, J. Eur. Acad. Dermatol. Venereol., 30, 1742, 10.1111/jdv.13674 · DOI
- Madanagobalane, 2012, The increased prevalence of non-alcoholic fatty liver disease in psoriatic patients: a study from South India, Australas. J. Dermatol., 53, 190, 10.1111/j.1440-0960.2012.00905.x · DOI
- de Matos, 2016, The effect of insulin resistance and exercise on the percentage of CD16(+) monocyte subset in obese individuals, Cell Biochem. Funct., 34, 209, 10.1002/cbf.3178 · DOI
- Roberts, 2015, The prevalence of NAFLD and NASH among patients with psoriasis in a tertiary care dermatology and rheumatology clinic, Aliment. Pharmacol. Ther., 41, 293, 10.1111/apt.13042 · DOI
- Jin, 2017, Serum human beta-defensin-2 is a possible biomarker for monitoring response to JAK inhibitor in psoriasis patients, Dermatology, 233, 164, 10.1159/000475809 · DOI
- Bracke, 2014, Targeted silencing of DEFB4 in a bioengineered skin-humanized mouse model for psoriasis: development of siRNA SECosome-based novel therapies, Exp. Dermatol., 23, 199, 10.1111/exd.12321 · DOI
- Erkin, 2007, Effect of PUVA, narrow-band UVB and cyclosporin on inflammatory cells of the psoriatic plaque, J. Cutan. Pathol., 34, 213, 10.1111/j.1600-0560.2006.00591.x · DOI · Paper page
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Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis
Li, X., Zang, Y., Li, X., Sheng, T., Liu, S., Chen, L., Xu, X., Wang, L., Long, R., Zhang, M., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-73278-8 · Cited by 1
Metadata
- Authors
- Nguyen, C. T. H., Kambe, N., Yamazaki, F., Ueda-Hayakawa, I., Kishimoto, I., & Okamoto, H.
- Venue
- Journal of Dermatological Science
- Publisher
- Elsevier BV
- Published
- 2018-05
- Volume
- 90
- Issue
- 2
- Pages
- 135-143
- ISSN
- 0923-1811
- Cited by
- 25
- References
- 1
- Language
- en
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