Cited by 17Genetic and Kidney Cyst DiseasesDermatology and Skin DiseasesPsoriasis: Treatment and Pathogenesis

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Increase in primary cilia in the epidermis of patients with atopic dermatitis and psoriasis

Open access

Abstract

Primary cilia influence cell activity, and thus have a unique role in maintaining cell proliferation and differentiation. In atopic dermatitis (AD) and psoriasis, areas of skin inflammation exhibit dysregulated keratinocyte homeostasis. The role of primary cilia in these conditions remains unclear. The objectives of this study is to elucidate the incidence of primary cilia in skin inflammation and the potential mechanism underlying the dysregulation of keratinocytes. Primary cilia were observed using immunofluorescence staining. Normal skin samples were compared with skin samples from patients with AD or psoriasis in terms of cilia numbers and length. The effect of cytokine stimulation on ciliogenesis in keratinocytes was analysed using a primary keratinocyte culture. IFT88, an important ciliary intraflagellar protein, was blocked in Th2 and Th17 cytokines‐stimulated keratinocytes. These effects were analysed with quantitative polymerase chain reaction and Western blot. Significant increases in ciliated cells were observed in AD and psoriasis skin samples compared with normal skin samples. The stimulation of keratinocytes using Th2 and Th17 cytokines modulated the formation of primary cilia. The amount of IFT88 in the primary cilia associated with the phosphorylation of JNK, but not p38, in keratinocytes stimulated with interleukin‐13, 17A and 22. An increase of ciliated cells in the epidermis may impair keratinocyte differentiation under stress conditions caused by inflammation in both AD and psoriasis patients.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1111/exd.14285

Cites

4 of 4 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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 Rizaldy et al. 2021

    The Discussion (page unavailable) reports a relationship between primary cilia and pro-inflammatory NFκB signaling in chondrocytes. The paper also finds that a cilia-related protein affects JNK phosphorylation in cytokine-stimulated keratinocytes, but it does not establish that primary cilia regulate immune responses broadly. (LLM, conf=0.78)

    Experimental — accuracy not yet measured
  • 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 Rizaldy et al. 2021

    The Results and Discussion report increased primary cilia in the epidermis of patients with atopic dermatitis and psoriasis, supporting a link between altered ciliation and these two inflammatory skin diseases. The paper does not establish primary-cilium defects across autoimmune and allergic diseases more broadly; it reports increased cilia rather than demonstrating a general defect. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 46

  1. 10.1016/j.jaci.2011.01.054 · DOI
  2. 10.1016/S0167-5699(98)01381-4 · DOI
  3. 10.1038/jid.2012.194 · DOI
  4. 10.1016/j.alit.2014.06.001 · DOI
  5. 10.1016/j.jaci.2011.01.053 · DOI
  6. 10.1038/jid.2008.111 · DOI
  7. 10.1016/j.coi.2017.08.008 · DOI
  8. 10.3389/fcell.2018.00008 · DOI · Paper page
  9. 10.1242/jcs.091256 · DOI
  10. 10.2174/138920211795860134 · DOI
  11. 10.1038/nmeth.2089 · DOI · Paper page
  12. Toriyama M, 2020, Immunological role of primary cilia of dendritic cells in human skin disease, bioRxiv
  13. 10.4172/2155-9899.1000110 · DOI
  14. 10.1016/j.jdermsci.2017.11.015 · DOI
  15. 10.1177/026119291103900508 · DOI
  16. 10.3389/fmed.2017.00119 · DOI
  17. 10.1038/jid.2013.503 · DOI
  18. 10.3390/cells9040857 · DOI
  19. 10.1038/jid.2014.124 · DOI
  20. 10.1016/j.cell.2011.05.030 · DOI
  21. 10.1038/labinvest.2010.81 · DOI
  22. 10.1038/cdd.2012.104 · DOI
  23. 10.1016/j.clim.2007.11.006 · DOI · Paper page
  24. 10.1016/j.jaci.2009.07.012 · DOI
  25. 10.1016/j.immuni.2015.07.007 · DOI · Paper page
  26. 10.1016/j.jid.2018.12.018 · DOI · Paper page
  27. 10.4049/jimmunol.174.6.3695 · DOI · Paper page
  28. 10.1111/j.1365-2133.2008.08769.x · DOI
  29. 10.1016/j.cellsig.2014.04.004 · DOI · Paper page
  30. 10.1016/j.joca.2019.03.003 · DOI
  31. 10.1007/s00018-013-1302-8 · DOI
  32. 10.1093/emboj/20.13.3427 · DOI
  33. 10.1074/jbc.M506119200 · DOI
  34. 10.1074/jbc.M602712200 · DOI
  35. 10.1172/JCI69071 · DOI
  36. 10.1101/cshperspect.a008383 · DOI
  37. 10.1002/path.3004 · DOI · Paper page
  38. 10.1038/ng.2739 · DOI
  39. 10.1590/abd1806-4841.20175709 · DOI
  40. 10.1002/cia2.12049 · DOI
  41. 10.1073/pnas.0406061101 · DOI
  42. 10.1038/sj.jid.5701184 · DOI
  43. 10.1242/jcs.122903 · DOI
  44. 10.1038/jid.2013.535 · DOI
  45. 10.1093/toxsci/kft215 · DOI
  46. 10.1016/S0923-1811(02)00064-6 · DOI

Cited by

Sorted by citations

Metadata

Authors
Rizaldy, D., Toriyama, M., Kato, H., Fukui, R., Fujita, F., Nakamura, M., Okada, F., Morita, A., & Ishii, K. J.
Affiliations
  • Bandung Institute of Technology (ID)
  • National Institute of Biomedical Innovation, Health and Nutrition (JP)
  • Nagoya City University (JP)
  • Mandom Corp. (Japan) (JP)
Corresponding author
  • Morita, Akimichi
  • Ishii, Ken J.
Venue
Experimental Dermatology
Publisher
Wiley
Published
2021-02-12
Volume
30
Issue
6
Pages
792-803
ISSN
  • 0906-6705 (ISSN-L)
  • 1600-0625
OpenAlex
W3124185010
Cited by
17
References
4
Citations by year
2026: 4 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 3 · 2021: 2
FWCI
1.55
Type
journal article
Language
en
Open access
Locations
  • Experimental Dermatology (publishedVersion)
  • PubMed (publishedVersion)
  • Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
  • NAIST Digital Library (Nara Institute of Science and Technology) (submittedVersion, cc-by-nc-nd)
Funders
  • Japan International Cooperation Agency
  • Nagoya City University
  • National Institutes of Biomedical Innovation, Health and Nutrition
  • Japan Society for the Promotion of Science (21K15087, 19K17797)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Kidney Cyst Diseases
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords
primary cilia, atopic dermatitis, psoriasis, keratinocytes, epidermis, ciliogenesis, IFT88, Th2 cytokines, Th17 cytokines, IL-13, IL-17A, IL-22, JNK phosphorylation, keratinocyte differentiation, skin inflammation
MeSH terms
Cells, Cultured, Cilia, Dermatitis, Atopic, Epidermis, Humans, Psoriasis, Keratinocytes, Cytokines

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 ›

Are you an author, or do you see a problem with this page? Request a review