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Dendritic cell proliferation by primary cilium in atopic dermatitis
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Introduction: Atopic dermatitis (AD) is a common allergic eczema that affects up to 10% of adults in developed countries. Immune cells in the epidermis, namely, Langerhans cells (LCs), contribute to the pathogenesis of AD, although their exact role(s) in disease remain unclear. Methods: We performed immunostaining on human skin and peripheral blood mononuclear cells (PBMCs) and visualized primary cilium. Result and discussion: We show that human dendritic cells (DCs) and LCs have a previously unknown primary cilium-like structure. The primary cilium was assembled during DC proliferation in response to the Th2 cytokine GM-CSF, and its formation was halted by DC maturation agents. This suggests that the role of primary cilium is to transduce proliferation signaling. The platelet-derived growth factor receptor alpha (PDGFRα) pathway, which is known for transducing proliferation signals in the primary cilium, promoted DC proliferation in a manner dependent on the intraflagellar transport (IFT) system. We also examined the epidermal samples from AD patients, and observed aberrantly ciliated LCs and keratinocytes in immature and proliferating states. Our results identify a potential relationship between the primary cilium and allergic skin barrier disorders, and suggest that targeting the primary cilium may contribute to treating AD.
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Recent evidence suggests a link between primary cilium defects and autoimmune and allergic diseases.
“Furthermore, recent evidence suggests a link between primary cilium defects and autoimmune and allergic diseases (Tsyklauri et al. 2021; Rizaldy et al. 2021; Toriyama et al. 2023; Toriyama and Ishii 2021).”
From Astrocyte-specific inhibition of the primary cilium suppresses C3 expression in reactive astrocyte (2024) · cites this paper as Toriyama et al. 2023
The primary cilium can regulate immune responses.
“These reports suggest that the primary cilium can regulate immune responses, although the role of the primary cilium in neuroinflammation remains largely unexplored.”
From Astrocyte-specific inhibition of the primary cilium suppresses C3 expression in reactive astrocyte (2024) · cites this paper as Toriyama et al. 2023
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Sorted by citations
Astrocyte-specific inhibition of the primary cilium suppresses C3 expression in reactive astrocyte
Muhamad, N. A., Masutani, K., Furukawa, S., Yuri, S., Toriyama, M., Matsumoto, C., Itoh, S., Shinagawa, Y., Isotani, A., Toriyama, M., et al. (2024) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-024-01482-5 · Cited by 9
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Metadata
- Authors
- Toriyama, M., Rizaldy, D., Nakamura, M., Atsumi, Y., Toriyama, M., Fujita, F., Okada, F., Morita, A., Itoh, H., & Ishii, K. J.
- Affiliations
- Kwansei Gakuin University (JP)
- Bandung Institute of Technology (ID)
- Nagoya City University (JP)
- National Institute of Biomedical Innovation, Health and Nutrition (JP)
- Mandom Corp. (Japan) (JP)
- Nara Institute of Science and Technology (JP)
- Corresponding author
- Toriyama, Manami
- Ishii, Ken J.
- ORCID
- Venue
- Frontiers in Molecular Biosciences
- Publisher
- Frontiers Media SA
- Published
- 2023-04-26
- Volume
- 10
- Pages
- 1149828-1149828
- ISSN
- 2296-889X (ISSN-L)
- PMC
- PMC10169737
- OpenAlex
- W4367053207
- Cited by
- 15
- References
- 2
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2023: 4
- FWCI
- 2.49
- Type
- journal article
- Language
- en
- Update notices
- corrigendum (2023-08-30)
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Molecular Biosciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Japan Society for the Promotion of Science (JP19K17797)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Kidney Cyst Diseases
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
- Keywords
- atopic dermatitis, primary cilia, dendritic cell proliferation, Langerhans cells, GM-CSF, PDGFRα signaling, intraflagellar transport, keratinocytes, ciliopathies
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