Cited by 27Psoriasis: Treatment and PathogenesisDermatology and Skin DiseasesSpondyloarthritis Studies and Treatments

Experimental Pharmacological Management of Psoriasis

Open access
Campione, Elena, Cosio, Terenzio, Di Prete, Monia, Lanna, Caterina, Dattola, Annunziata, Bianchi, Luca·2021·Journal of Experimental Pharmacology

Abstract

Psoriasis is a chronic, relapsing, immune-mediated systemic disease. Its pathogenesis is complex and not fully understood yet. Genetic and epigenetic factors interact with molecular pathways involving TNF-α, IL-23/IL-17 axis, and peculiar cytokines, as IL-36 or phosphodiesterase 4. This review discusses the mechanisms involved in the development of the disease, as well as the therapeutic options proposed following the investigation of the inflammatory psoriatic pathways. We performed a comprehensive search using the words "psoriasis" and the newest molecules currently under investigation and approval. From these data, a new scenario in psoriasis is occurring to personalize the therapies - especially systemic ones and those using small molecules - and avoid topical and injectable drugs. We reported the newest therapeutic opportunities, including the inhibitors of Janus kinase/tyrosine kinase 2, phosphodiesterase-4 and IL-36 receptor. Today, more than 20 molecules are under investigation for the treatment of cutaneous psoriasis. Most of them are constituted by small molecules or biologic therapies. This underlines how psoriasis needs systemic therapies, due to its complex pathogenesis and multisystemic involvement.

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Crossref · 10.2147/jep.s265632

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  • Therapies targeting IL-17, including monoclonal antibodies against IL-17A or its receptor, produce rapid and efficient clinical responses in psoriasis by suppressing keratinocyte activation and neutrophil recruitment, which are key downstream effects of Th17 immunity.

    “Therapies targeting IL-17 (monoclonal antibodies against IL-17A or its receptor) have shown rapid and efficient clinical responses by directly suppressing keratinocyte activation and neutrophil recruitment, which are key downstream effects of Th17 immunity.”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [29]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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  • Selective IL-23 inhibitors show high efficacy with durable responses in psoriasis, likely by disrupting the maintenance of disease-driving Th17 cells.

    “selective IL-23 inhibitors have also shown high efficacy with durable responses, likely by disrupting the maintenance of disease-driving Th17 cells [29,30,31,32].”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [29]

    The Discussion (page unavailable) says IL-23 promotes Th17-cell differentiation and proliferation, supporting the proposed mechanism in broad terms. But the paper discusses inhibitors of JAK/TYK2 signalling involving IL-23, not selective IL-23 inhibitors, and does not establish their high efficacy or durable responses. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • The IL-23/Th17 axis is a central driver of psoriasis.

    “The identification of the IL-23/Th17 axis as a central driver of psoriasis has led to the development of biologic therapies that selectively interrupt cytokine networks.”
  • IL-23 is an upstream regulator of pathogenic T-cell populations in psoriasis.

    “Furthermore, increasing evidence supports IL-23 as an upstream regulator of pathogenic T-cell populations; thus, selective IL-23 inhibitors have also shown high efficacy with durable responses, likely by disrupting the maintenance of disease-driving Th17 cells [29,30,31,32].”

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Authors
Campione, E., Cosio, T., Di Prete, M., Lanna, C., Dattola, A., & Bianchi, L.
Affiliations
University of Rome Tor Vergata (IT)
Corresponding author
Campione, Elena
Venue
Journal of Experimental Pharmacology
Published
2021-07
Volume
Volume 13
Pages
725-737
ISSN
1179-1454 (ISSN-L)
OpenAlex
W3186757904
Cited by
27
References
91
Citations by year
2026: 6 · 2025: 4 · 2024: 3 · 2023: 7 · 2022: 7
FWCI
0.44
Type
journal article
Language
en
Open access
Locations
  • Journal of Experimental Pharmacology (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by-nc)
  • Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
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, psoriasis pathogenesis, TNF-α, IL-23/IL-17 axis, IL-36, phosphodiesterase 4, JAK inhibitors, tyrosine kinase inhibitors, IL-36 receptor antagonist, small molecule therapy, biologic therapy, personalized treatment, systemic therapy

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