Mast Cells and Neutrophils Release IL-17 through Extracellular Trap Formation in Psoriasis
Open accessAbstract
IL-17 and IL-23 are known to be absolutely central to psoriasis pathogenesis because drugs targeting either cytokine are highly effective treatments for this disease. The efficacy of these drugs has been attributed to blocking the function of IL-17–producing T cells and their IL-23–induced expansion. However, we demonstrate that mast cells and neutrophils, not T cells, are the predominant cell types that contain IL-17 in human skin. IL-17+ mast cells and neutrophils are found at higher densities than IL-17+ T cells in psoriasis lesions and frequently release IL-17 in the process of forming specialized structures called extracellular traps. Furthermore, we find that IL-23 and IL-1β can induce mast cell extracellular trap formation and degranulation of human mast cells. Release of IL-17 from innate immune cells may be central to the pathogenesis of psoriasis, representing a fundamental mechanism by which the IL-23–IL-17 axis mediates host defense and autoimmunity.
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IL-17, produced primarily by CD4+ Th17 cells, acts to enhance chemokine production by target cells in various tissues to promote/attract monocytes and neutrophils to those tissue (especially mucosal) sites, and in combination with sICAM suggests the predominance of a Th1 phenotypic response (acute pro-inflammatory state).
“IL-17, produced primarily by CD4+ Th17 cells, acts to enhance chemokine production by target cells in various tissues to promote/attract monocytes and neutrophils to those tissue (especially mucosal) sites, and in combination with sICAM suggests the predominance of a Th1 phenotypic response (acute pro-inflammatory state) [25-30].”
From Oral neutrophils are an independent marker of the systemic inflammatory response after cardiac bypass (2014) · cites this paper as [30]
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“IL-17, produced primarily by CD4+ Th17 cells, acts to enhance chemokine production by target cells in various tissues to promote/attract monocytes and neutrophils to those tissue (especially mucosal) sites, and in combination with sICAM suggests the predominance of a Th1 phenotypic response (acute pro-inflammatory sta…”
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- Authors
- Lin, A. M., Rubin, C. J., Khandpur, R., Wang, J. Y., Riblett, M., Yalavarthi, S., Villanueva, E. C., Shah, P., Kaplan, M. J., & Bruce, A. T.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Khandpur, Ritika
- Riblett, MaryBeth
- Shah, Parth
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-07-01
- Volume
- 187
- Issue
- 1
- Pages
- 490-500
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3119764
- OpenAlex
- W2096620879
- Cited by
- 906
- References
- 66
- Citations by year
- 2026: 27 · 2025: 39 · 2024: 57 · 2023: 43 · 2022: 56 · 2021: 72 · 2020: 72 · 2019: 75 · 2018: 62 · 2017: 75 · 2016: 79 · 2015: 65 · 2014: 68 · 2013: 59 · 2012: 47
- FWCI
- 26.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Michigan
- National Institutes of Health (2t32ar007197-46a1)
- National Heart, Lung, and Blood Institute (R01HL088419)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (T32-AR007197, 5T32AR007197-33)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Keywords
- psoriasis, mast cells, neutrophils, IL-17, extracellular traps, neutrophil extracellular traps, IL-23, IL-1β, mast cell degranulation, innate immune cells, autoimmunity, skin lesions
- MeSH terms
- Extracellular Space, Humans, Immunity, Innate, Leukocyte Count, Mast Cells, Neutrophils, Psoriasis, Skin, T-Lymphocyte Subsets, Interleukin-17, Tryptases, Chymases
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