Evidence map›Paper›PMID 39283337›Full record

ArticleMycopathologia2024

Malassezia globosa Induces Differentiation of Pathogenic Th17 Cells by Inducing IL-23 Secretion by Keratinocytes.

Qiuyu Jia, Jian Hu, Xiaojie Wang, Yuxuan Deng, Jianzhong Zhang, Houmin Li

Abstract read
PubMed Publisher
In one paragraph

Article in Mycopathologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. A review of core immuno-inflammatory mechanisms and key regulatory targets in psoriasis.American journal of clinical and experimental immunology · 2026
    Review
  7. Microbiome dysbiosis and therapeutic restoration in atopic dermatitis.Frontiers in cellular and infection microbiology · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Seborrheic Dermatitis: Exploring the Complex Interplay withInternational journal of molecular sciences · 2025
    Review
  13. Article
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Qiuyu Jia *Department of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
Jian Hu *Department of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
Xiaojie WangDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
Yuxuan DengDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
Jianzhong ZhangDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
Houmin LiDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China. lhoumin@sina.cn.

Funding

National Natural Science Foundation of China 81772160Natural Science Foundation of Beijing Municipality 7222195
6 · The paper itself

Abstract

Malassezia, the most abundant fungal commensal on the mammalian skin, has been linked to several inflammatory skin diseases such as atopic dermatitis, seborrheic dermatitis and psoriasis. This study reveals that epicutaneous application with Malassezia globosa (M. globosa) triggers skin inflammation in mice. RNA-sequencing of the resulting mouse lesions indicates activation of Interleukin-17 (IL-17) signaling and T helper 17 (Th17) cells differentiation pathways by M. globosa. Furthermore, our findings demonstrate a significant upregulation of IL-23, IL-23R, IL-17A, and IL-22 expressions, along with an increase in the proportion of Th17 and pathogenic Th17 cells in mouse skin exposed to M. globosa. In vitro experiments illustrate that M. globosa prompts human primary keratinocytes to secrete IL-23 via TLR2/MyD88/NF-κB signaling. This IL-23 secretion by keratinocytes is shown to be adequate for inducing the differentiation of pathogenic Th17 cells in the skin. Overall, these results underscore the significant role of Malassezia in exacerbating skin inflammation by stimulating IL-23 secretion by keratinocytes and promoting the differentiation of pathogenic Th17 cells.

Indexed as

Interleukin-23KeratinocytesMalasseziaTh17 CellsAnimalsCell DifferentiationCells, CulturedDermatomycosesHumansMiceMice, Inbred C57BLMyeloid Differentiation Factor 88NF-kappa BSignal TransductionToll-Like Receptor 2Interleukin-23Myeloid Differentiation Factor 88NF-kappa BToll-Like Receptor 2IL-23Malassezia globosaMyD88NF-κBTh17 cellsTLR2

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.