Etiology and Pathogenesis of Psoriasis
Abstract
Psoriasis is a common, chronic inflammatory skin disease most often appearing in the form of well-demarcated, scaly plaques. These lesions highlight the fundamental processes underlying its pathogenesis, namely, inflammation and epidermal hyperproliferation. Both phenomena are considered consequences of an intimate interplay between the innate and the adaptive immune system. This concept is supported by results of genetic studies, pointing toward the signaling pathways of nuclear factor-κB, interferon-γ, and interleukin (IL)-23 as well as antigen presentation as central axes of the psoriatic inflammation. Efficacy of biologics targeting tumor necrosis factor-α, IL-23, or IL-17 provides further evidence in favor of this model.
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Psoriasis lesions are thicker and present as plaques sharply limited with silvery white scales.
“While psoriasis can affect similar locations as SD, typical lesions in psoriasis are thicker and present as plaques sharply limited with silvery white scales [8,32].”
From Seborrheic Dermatitis and Dandruff: A Comprehensive Review (2015) · cites this paper as [32]
Cites
Secukinumab in plaque psoriasis—results of two phase 3 trials
Langley, R. G., Elewski, B. E., Lebwohl, M., Reich, K., Griffiths, C. E. M., Papp, K., Puig, L., Nakagawa, H., Spelman, L., Sigurgeirsson, B., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1314258 · Cited by 1,997 · see citing works
Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide
Lande, R., Gregorio, J., Facchinetti, V., Chatterjee, B., Wang, Y.-H., Homey, B., Cao, W., Wang, Y.-H., Su, B., Nestle, F. O., et al. (2007) · Nature · doi:10.1038/nature06116 · Cited by 1,910 · see citing works
Risk of myocardial infarction in patients with psoriasis
Gelfand, J. M., Neimann, A. L., Shin, D. B., Wang, X., Margolis, D. J., & Troxel, A. B. (2006) · JAMA · doi:10.1001/jama.296.14.1735 · Cited by 1,899 · see citing works
Kebir, H., Kreymborg, K., Ifergan, I., Dodelet-Devillers, A., Cayrol, R., Bernard, M., Giuliani, F., Arbour, N., Becher, B., & Prat, A. (2007) · Nature Medicine · doi:10.1038/nm1651 · Cited by 1,759 · see citing works
Wolf, N., Quaranta, M., Prescott, N. J., Allen, M., Smith, R., Burden, A. D., Worthington, J., Griffiths, C. E. M., Mathew, C. G., Barker, J. N., et al. (2008) · Journal of Medical Genetics · doi:10.1136/jmg.2007.053595 · Cited by 171 · see citing works
Innate immunity and antimicrobial defense systems in psoriasis
Büchau, A. S., & Gallo, R. L. (2007) · Clinics in Dermatology · doi:10.1016/j.clindermatol.2007.08.016 · Cited by 169 · see citing works
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Seborrheic Dermatitis and Dandruff: A Comprehensive Review
(2015) · Journal of Clinical and Investigative Dermatology · doi:10.13188/2373-1044.1000019 · Cited by 398 · see citing works
- Authors
- Boehncke, W.-H.
- Affiliations
- University of Geneva (CH)
- Corresponding author
- Boehncke, Wolf-Henning
- Venue
- Rheumatic Disease Clinics of North America
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 41
- Issue
- 4
- Pages
- 665-675
- ISSN
- 0889-857X (ISSN-L)
- OpenAlex
- W1826301003
- Cited by
- 197
- References
- 6
- Citations by year
- 2026: 6 · 2025: 12 · 2024: 14 · 2023: 20 · 2022: 26 · 2021: 21 · 2020: 28 · 2019: 27 · 2018: 17 · 2017: 12 · 2016: 11 · 2015: 2
- FWCI
- 1.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Rheumatic Disease Clinics of North America (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Rheumatology › Spondyloarthritis Studies and Treatments
- Keywords
- psoriasis, pathogenesis, etiology, epidermal hyperproliferation, skin inflammation, innate-adaptive immune interaction, genetic susceptibility, NF-κB signaling, interferon-gamma, IL-23, antigen presentation, biologic therapy, TNF-α, IL-17
- MeSH terms
- Humans, Inflammation, Psoriasis, Skin, Cytokines, Adaptive Immunity
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