HLA-Cw1 and Psoriasis
Open accessAbstract
Psoriasis is a chronic inflammatory skin condition with regional and ethnic differences in its prevalence and clinical manifestations. Human leukocyte antigen (HLA)-Cw6 is the disease allele conferring the greatest risk to psoriasis, but its prevalence is lower in Asian individuals. Recent studies have found associations between HLA-Cw1 and some Asian populations with psoriasis, especially Southern Chinese. HLA-Cw6 was associated with type I early-onset psoriasis, guttate psoriasis, Koebner phenomenon, and better response to methotrexate, interleukin (IL)-12/23, IL-17, and IL-23 targeting drugs. In contrast, HLA-Cw1 positivity has been associated with erythrodermic psoriasis, pustular psoriasis, and the axial type of psoriatic arthritis. Furthermore, HLA-Cw1 was more frequently associated with high-need patients who did not respond to conventional therapies. No known trigger factor nor autoantigen has been identified for HLA-Cw1 positivity. However, HLA-Cw1 has been linked to some viral agents. For example, cytotoxic T lymphocytes recognize multiple cytomegalovirus pp65-derived epitopes presented by HLA alleles, including HLA-C*01:02. In addition, cytomegalovirus can lead to severe exacerbation of psoriatic skin disease. The proposed interaction between viral infection, HLA-Cw1, and psoriasis is through the killer cell immunoglobulin-like receptors of natural killer cells. Given the diverse nature of psoriasis pathogenesis and the difference in HLA-Cw prevalence in different racial groups, more studies are needed to confirm the role of HLA-Cw1 in psoriasis.
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These cytokines occupy key positions in the dominant pathogenic circuit described in recent psoriasis literature.
“These cytokines occupy key positions in the dominant pathogenic circuit described in recent psoriasis literature [22,23,24].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [24]
The Introduction (page unavailable) links psoriasis susceptibility to activation of T helper-17 cells, and the Conclusions table lists treatments targeting IL-12/23, IL-17, and IL-23. These passages connect those cytokines to psoriasis, but they do not describe their positions in a dominant pathogenic circuit. (LLM, conf=0.75)
Experimental — accuracy not yet measuredThis mechanistic framework explains the efficacy of biologic therapies targeting TNF, IL-17, and IL-23, which interrupt key nodes in the pathogenic network.
“This mechanistic framework explains the efficacy of biologic therapies targeting TNF, IL-17, and IL-23, which interrupt key nodes in the pathogenic network.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [24]
The “HLA-Cw1 and Clinical Presentations of Psoriasis” section (page unavailable) reports responses to anti-IL-17 and anti-IL-23 drugs in HLA-Cw6-positive patients, but says anti-TNF agents showed less efficacy in that group. The paper does not connect these treatment responses to interruption of TNF, IL-17, and IL-23 nodes in a pathogenic network, so it supports the treatment-response point only in a narrower form. (LLM, conf=0.84)
Experimental — accuracy not yet measuredCell interactions in psoriasis are a tightly coordinated circuit between keratinocytes, dendritic cells, T cells, and innate immune populations.
“Cell interactions in psoriasis are a tightly coordinated circuit between keratinocytes, dendritic cells, T cells, and innate immune populations.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [24]
The Introduction describes altered keratinocyte differentiation alongside inflammatory-cell infiltration and T-cell and NK-cell involvement. “Role of HLA-Cw1 in the Immune System” describes LL-37 activating dendritic cells and contributing to a pathogenic T-cell response. These passages support interactions among several named cell types, but do not establish a tightly coordinated circuit linking all four populations, particularly keratinocytes. (LLM, conf=0.82)
Experimental — accuracy not yet measuredAs psoriatic inflammation persists, lesions become self-sustaining through IL-23 maintaining pathogenic lymphocytes, IL-17 and IL-22 reshaping the epidermis, TNF-α amplifying the inflammatory network, and angiogenic factors such as VEGF remodeling the microvasculature.
“As this inflammatory process persists, the lesions become self-sustaining: IL-23 maintains pathogenic lymphocytes, IL-17 and IL-22 reshape the epidermis, TNF-α amplifies the inflammatory network, and angiogenic factors such as VEGF remodel the microvasculature.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [24]
The Introduction describes psoriasis as an inflammatory disease involving immune-cell infiltration and altered keratinocyte differentiation, and Table 2 in the Conclusions mentions treatments targeting IL-23, IL-17, and TNF. Neither passage explains the claimed roles of those cytokines, addresses IL-22 or VEGF, or says that lesions become self-sustaining through microvascular remodeling. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe psoriatic process is initiated by stress-activated keratinocytes, which release antimicrobial peptides, cytokines, and nucleic acid complexes that activate plasmacytoid and myeloid dendritic cells, leading to type I interferon production and subsequent IL-23 and TNF-α secretion.
“The process is initiated by stress-activated keratinocytes, which release antimicrobial peptides, cytokines, and nucleic acid complexes that activate plasmacytoid and myeloid dendritic cells, leading to type I interferon production and subsequent IL-23 and TNF-α secretion [19,24].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [24]
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Tinca, A. C., Cozac-Szoke, A. R., & Cotoi, O. S. (2026) · Dermatopathology · doi:10.3390/dermatopathology13020022 · Cited by 1 · see citing works
“These cytokines occupy key positions in the dominant pathogenic circuit described in recent psoriasis literature [22–24].”
- Authors
- Huang, Y.-W., & Tsai, T.-F.
- Affiliations
- National Taiwan University Hospital (TW)
- National Taiwan University (TW)
- Corresponding author
- Tsai, Tsen-Fang
- Venue
- American Journal of Clinical Dermatology
- Published
- 2021-01-18
- Volume
- 22
- Issue
- 3
- Pages
- 339-347
- ISSN
- 1175-0561 (ISSN-L)
- 1179-1888
- PMC
- PMC7812566
- OpenAlex
- W3124643655
- Cited by
- 62
- References
- 98
- Citations by year
- 2026: 10 · 2025: 18 · 2024: 14 · 2023: 10 · 2022: 9 · 2021: 1
- FWCI
- 0.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal of Clinical Dermatology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Rheumatology › Spondyloarthritis Studies and Treatments
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Keywords
- HLA-Cw1, psoriasis, HLA-Cw6, genetic susceptibility, Asian populations, Southern Chinese, erythrodermic psoriasis, pustular psoriasis, psoriatic arthritis, guttate psoriasis, methotrexate response, IL-23 inhibitors, IL-17 inhibitors, IL-12/23 inhibitors, cytomegalovirus, viral triggers, natural killer cells, killer cell immunoglobulin-like receptors, ethnic differences
- MeSH terms
- Alleles, Gene Frequency, Humans, Killer Cells, Natural, Psoriasis, Severity of Illness Index, Skin, Genetic Variation, Virus Diseases, HLA-C Antigens, Arthritis, Psoriatic, Comorbidity, Genetic Predisposition to Disease, Asian People
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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