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Innate immunity and antimicrobial defense systems in psoriasis
Open accessAbstract
Psoriasis is a chronic inflammatory disorder that is mediated by elements of the innate and adaptive immune systems. Its characteristic features in the skin consist of inflammatory changes in both dermis and epidermis, with abnormal keratinocyte differentiation and proliferation. Despite the elucidation of many aspects of psoriasis pathogenesis, some puzzling questions remain to be answered. A major question currently debated is whether psoriasis is a primary abnormality of the epidermal keratinocyte or a reflection of dysregulated bone marrow-derived immunocytes. In this review we will focus on understanding the role of the innate immune system in psoriasis and how this provides a rational solution to address the origin of this multifactorial disease. Innate immunity is nonspecific and genetically based. It protects the body against the constant risk of pathogens through the use of rapidly mobilized defenses that are able to recognize and kill a variety of threats (bacteria, fungi, viruses, etc). The key mechanisms of innate immune responses are the existence of receptors to recognize pathogens and the production of factors that kill pathogens, such as antimicrobial peptides and proteins. Any combination of excessive sensitivity of the innate detection system, or dysregulation of the response system, can manifest both an epidermal phenotype and an abnormal T-cell function. Thus, the multidimensional action of the innate immune system, its triggers, and its recently understood role in T-cell function argue for an important role for innate mechanisms of recognition and response in the pathogenesis of psoriasis.
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“IL-1, TNFα, IFNγ, IL-17, and IL-22 are strong inducers of hBD2 and hBD3 expression.25,36,39”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [36]
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“AMPs can amplify the proinflammatory cytokine response and can thus, in some circumstances, assume pathogenic roles as in psoriasis, rosacea, and other skin diseases.36–38”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [36]
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“Furthermore, hBD2 expression is induced by high calcium concentrations and 1,25 vitamin D3.36”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [36]
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“IL-17A and IL-22 are two members of the cytokine family with substantial roles in host defense and other immunoregulatory functions.25,36,39,69–72”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [36]
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Sorted by citations
Nestle, F. O., Kaplan, D. H., & Barker, J. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0804595 · Cited by 2,867
Boehncke, W., & Schön, M. P. (2015) · The Lancet · doi:10.1016/s0140-6736(14)61909-7 · Cited by 2,609
Kryczek, I., Bruce, A. T., Gudjonsson, J. E., Johnston, A., Aphale, A., Vatan, L., Szeliga, W., Wang, Y., Liu, Y., Welling, T. H., et al. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.181.7.4733 · Cited by 474
Pathogenesis of psoriasis and development of treatment
Ogawa, E., Sato, Y., Minagawa, A., & Okuyama, R. (2017) · The Journal of Dermatology · doi:10.1111/1346-8138.14139 · Cited by 470
The Interplay Between Keratinocytes and Immune Cells in the Pathogenesis of Psoriasis
Albanesi, C., Madonna, S., Gisondi, P., & Girolomoni, G. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01549 · Cited by 432
Metadata
- Authors
- Büchau, A. S., & Gallo, R. L.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Gallo, Richard L.
- ORCID
- Gallo, Richard L.
- Venue
- Clinics in Dermatology
- Publisher
- Elsevier BV
- Published
- 2007-11
- Volume
- 25
- Issue
- 6
- Pages
- 616-624
- ISSN
- 0738-081X (ISSN-L)
- PMC
- PMC2699547
- OpenAlex
- W2164880184
- Cited by
- 169
- References
- 95
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 14 · 2023: 11 · 2022: 9 · 2021: 9 · 2020: 10 · 2019: 7 · 2018: 11 · 2017: 9 · 2016: 11 · 2015: 9 · 2014: 11 · 2013: 8 · 2012: 11
- FWCI
- 0.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Clinics in Dermatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R21AI048176, R01AI052453, R37AI052453)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR052728, R29AR044379, R01AR045676, R01AR044379)
- 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, innate immunity, antimicrobial peptides, antimicrobial defense, pathogen recognition receptors, keratinocyte differentiation, T cell dysfunction, skin inflammation, psoriasis pathogenesis
- MeSH terms
- Bacterial Infections, Humans, Immunity, Active, Immunity, Cellular, Immunity, Innate, S100 Proteins, Psoriasis, Skin, Cytokines, Antimicrobial Cationic Peptides, Toll-Like Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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