Cited by 170Psoriasis: Treatment and PathogenesisDermatology and Skin DiseasesSpondyloarthritis Studies and Treatments

Innate immunity and antimicrobial defense systems in psoriasis

Open access
Büchau, Amanda S., Gallo, Richard L.·2007·Clinics in Dermatology

Abstract

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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Registry

Crossref · 10.1016/j.clindermatol.2007.08.016

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94 of 94 references verified0 citation errors · 0 not checkable

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  • IL-1, TNFα, IFNγ, IL-17, and IL-22 are strong inducers of hBD2 and hBD3 expression.

    “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]

  • AMPs can amplify the proinflammatory cytokine response and can thus, in some circumstances, assume pathogenic roles as in psoriasis, rosacea, and other skin diseases.

    “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]

  • hBD2 expression is induced by high calcium concentrations and 1,25 vitamin D3.

    “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]

  • IL-17A and IL-22 have substantial roles in host defense and immunoregulatory functions.

    “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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1 of the 95 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. [83]Büchau AS, Kukova G, Lewerenz V, Wolf R, Ruzicka T, Walz M. Human S100A15 is regulated by calcium, cytokines, and bacterial compounds. J Invest Dermatol. 2006;126(supplement 4):69. [Google Scholar]

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Authors
Büchau, A. S., & Gallo, R. L.
Affiliations
University of California San Diego (US)
Corresponding author
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)
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
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

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