Cited by 75Psoriasis: Treatment and PathogenesisT-cell and B-cell ImmunologyRheumatoid Arthritis Research and Therapies

Th17 cell pathogenicity in autoimmune disease

Open access
Park, Eunchong, Ciofani, Maria·2025·Experimental & Molecular Medicine

Abstract

T helper 17 (Th17) cells have been implicated in numerous inflammatory autoimmune diseases. Clinical benefits from targeting Th17 cell-related cytokines, such as IL-17 and IL-23, highlight how knowledge of Th17 cell development and effector function can be translated into treatments for inflammatory disease. Here we discuss the pathogenic roles of Th17 cells in autoimmune diseases such as multiple sclerosis, inflammatory bowel disease and psoriasis, with emphasis on the cytokines, transcriptional regulators and metabolites that influence Th17 cell differentiation and pathogenicity. Moreover, we address how intestinal environments and physiological responses affect Th17 cells in autoimmune diseases. We also examine current and emerging therapeutic strategies aimed at regulating Th17 cell-driven inflammation to mitigate autoimmune diseases.

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Crossref · 10.1038/s12276-025-01535-9

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  • Factors such as VEGF induce endothelial activation, vascular dilation, and neovascularization in the papillary dermis, facilitating sustained leukocyte migration into the skin.

    “Factors such as VEGF induce endothelial activation, vascular dilation, and neovascularization in the papillary dermis, facilitating sustained leukocyte migration into the skin [27].”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [27]

    The psoriasis passage in “Th17 cell pathogenicity in autoimmune diseases” (page unavailable) says that inflammatory cytokines and chemokines recruit neutrophils to inflamed skin. It does not attribute that recruitment to VEGF or describe endothelial activation, vascular dilation, neovascularization in the papillary dermis, or sustained migration. (LLM, conf=0.76)

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  • Increasing real-world evidence supports the durable efficacy and favorable long-term disease control achieved with selective IL-23 inhibitors.

    “Increasing real-world evidence also supports the durable efficacy and favorable long-term disease control achieved with selective IL-23 inhibitors [27,28].”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [27]

    The “Antibodies: cytokine blockade” section says selective IL-23-blocking antibodies demonstrate therapeutic efficacy in autoimmune diseases, including psoriasis and IBD. It does not report increasing real-world evidence, durable efficacy, or long-term disease control; it also notes resistance to IL-23 blockade in some Th17 cell populations. No page number is available in our copy. (LLM, conf=0.87)

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  • Throughout the psoriatic process, continuous exchange between keratinocytes and immune cells maintains a loop in which IL-23 sustains pathogenic T cells, IL-17 and IL-22 perpetuate epidermal alterations, and TNF-α amplifies inflammation across multiple cell types.

    “Throughout this process, continuous exchange between keratinocytes and immune cells maintains a loop in which IL-23 sustains pathogenic T cells, IL-17 and IL-22 perpetuate epidermal alterations, and TNF-α amplifies inflammation across multiple cell types.”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [27]

    Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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Authors
Park, E., & Ciofani, M.
Affiliations
  • AstraZeneca (United States) (US)
  • Duke University (US)
Corresponding author
Ciofani, Maria
Venue
Experimental & Molecular Medicine
Published
2025-09-01
Volume
57
Issue
9
Pages
1913-1927
ISSN
  • 1226-3613 (ISSN-L)
  • 2092-6413
OpenAlex
W4413865457
Cited by
75
References
280
Citations by year
2026: 70 · 2025: 5
FWCI
6.71
Type
journal article
Language
en
Open access
Locations
  • Experimental & Molecular Medicine (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (AI156186)
  • U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (GM115474)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
Keywords
Th17 cells, autoimmune disease, IL-17, IL-23, Th17 cell differentiation, multiple sclerosis, inflammatory bowel disease, psoriasis, transcription factors, metabolites, intestinal environment, anti-inflammatory therapy
MeSH terms
Animals, Autoimmune Diseases, Cell Differentiation, Disease Susceptibility, Humans, Cytokines, Th17 Cells

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