Review of bimekizumab in the treatment of psoriasis
Open accessAbstract
Bimekizumab, a selective interleukin (IL) 17 inhibitor, is an emerging systemic treatment for moderate-to-severe psoriasis. Although IL-19, IL-22, and IL-36 are implicated in the pathogenesis of psoriasis, IL-17 drives the activation of these interleukins and the formation of psoriatic plaques. This review assesses the efficacy, safety, and implications of bimekizumab in the treatment of moderate-to-severe psoriasis. A review of literature was conducted using the PubMed repository in March 2022. Articles in English discussing the use of bimekizumab in the treatment of psoriasis were included. One phase II and four phase III trials were included. During clinical trials, bimekizumab was more efficacious, when compared to placebo, ustekinumab, adalimumab, and secukinumab in the treatment of moderate to severe psoriasis. Bimekizumab is a promising, efficacious, and relatively tolerable emerging systemic treatment for moderate-to-severe plaque psoriasis.
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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.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [30]
The 'Basis in pathology' section (page unavailable) says Th17 cells produce IL-17 and that IL-17 is crucial to psoriatic plaque formation. The 'IL-17 inhibitors' section says IL-17 is a major cytokine in psoriasis and that biologics selectively target it. The review lists IL-23 inhibitors, but does not explain or identify the IL-23/Th17 axis as a central driver. (LLM, conf=0.82)
Experimental — accuracy not yet measuredSelective 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 [30]
The Advantages/disadvantages section describes IL-23 inhibitors as efficacious for psoriasis and reports favorable PASI90 results for risankizumab and guselkumab. It does not establish durable responses or say that IL-23 inhibition disrupts the maintenance of disease-driving Th17 cells; its discussion of Th17 cells in Basis in pathology does not make that connection. Page numbers were not available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredTherapies 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 [30]
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Experimental — accuracy not yet measuredPsoriasis histopathological findings reflect activation of the IL-23/Th17 axis.
“These reflect activation of the IL-23/Th17 axis.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [30]
The “Basis in pathology” section (page unavailable) links Th17 activation and IL-17 activity to psoriatic plaques and epidermal hyperplasia. It does not explicitly link the histopathological findings to activation of the full IL-23/Th17 axis; IL-23 appears in the supplied passages only in treatment classes and references. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIn psoriasis, histopathological findings include acanthosis, parakeratosis, neutrophilic microabscesses, and prominent dermal vascular proliferation.
“In psoriasis, histopathological findings include acanthosis, parakeratosis, neutrophilic microabscesses, and prominent dermal vascular proliferation.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [30]
The “Basis in pathology” section (page unavailable) describes keratinocyte proliferation and epidermal hyperplasia, which support the acanthosis component. It does not describe parakeratosis, neutrophilic microabscesses, or prominent dermal vascular proliferation. (LLM, conf=0.83)
Experimental — accuracy not yet measured
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].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [30]
The ‘Basis in pathology’ section describes activation of Th17 cells by myeloid dendritic cells and identifies IL-17 as a contributor to psoriasis, but it does not say IL-23 regulates those cells. Searches for IL-23 as an upstream regulator or maintainer of Th17 cells found only mentions of IL-23 inhibitors and a reference title, not a passage making the claimed connection. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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- Authors
- Koppu, S., Singh, R., Kaur, K., & Feldman, S. R.
- Affiliations
- Wake Forest University Health Sciences (US)
- Corresponding author
- Singh, Rohan
- Venue
- Human Vaccines & Immunotherapeutics
- Publisher
- Informa UK Limited
- Published
- 2022-09-12
- Volume
- 18
- Issue
- 6
- Pages
- 2119767-2119767
- ISSN
- 2164-5515 (ISSN-L)
- 2164-554X
- PMC
- PMC9746354
- OpenAlex
- W4295886153
- Cited by
- 11
- References
- 24
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 3 · 2023: 2
- FWCI
- 0.76
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Human Vaccines & Immunotherapeutics (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- no funding
- 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
- bimekizumab, psoriasis, IL-19, IL-22, IL-36, systemic therapy, drug efficacy, drug safety, ustekinumab, adalimumab, secukinumab
- MeSH terms
- Ustekinumab, Antibodies, Monoclonal, Humans, Psoriasis, Severity of Illness Index, Treatment Outcome
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