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Th17 cell pathogenicity in autoimmune disease
Open accessAbstract
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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“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]
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“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]
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“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]
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Metadata
- 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
- PMC
- PMC12508148
- OpenAlex
- W4413865457
- Cited by
- 75
- References
- 280
- Citations by year
- 2026: 70 · 2025: 5
- FWCI
- 6.71
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- 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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