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Peer-reviewedCC BY 4.0Frontiers in Immunology

House dust mite drives biphasic immunomodulation of inflammatory dendritic epidermal cells via glucose metabolism in atopic dermatitis

  • Ying Zhao1,2
  • Cuie Gao1,2
  • Xin Sui1,2
  • Lan Ge1,2
  • Huan Wang1,2
  • Sisi Deng1,2
  • Qiquan Chen1,2
  • Lu Liu1,2
  • Jing Tian1,2
  • Tong Mu1,2
  • Li Wang3
  • Zhiqiang Song1,2
  1. 1Department of Dermatology, The First Affiliated Hospital (Southwest Hospital) of Army Medical University, Chongqing, China
  2. 2Chongqing Municipal Health Commission Key Laboratory of Immunological Skin Diseases, Chongqing, China
  3. 3Institute of Immunology, College of Basic Medical Sciences, Army Medical University, Chongqing, China
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Abstract

Background: The impact of environmental antigens, specifically house dust mite (HDM) and Staphylococcus aureus enterotoxin B (SEB), on the metabolism of inflammatory dendritic epidermal cells (IDECs) and its role in atopic dermatitis (AD) pathogenesis is poorly understood. This study aimed to characterize IDECs metabolism in AD and study how antigen exposure drives metabolic reprogramming and immune responses.

Methods: We first analyzed the single-cell RNA transcriptome sequencing data to explore metabolic profiles in IDECs from AD patients. Subsequently, we evaluated the effects of HDM alone or in combination with SEB for 24 h on the energy metabolism, maturation and cytokines secretion of monocytes-derived IDECs (moIDECs) in vitro. Finally, we investigated the dynamic changes of functional and glucose metabolism in moIDECs in vitro treated with HDM at different time points (6 h, 24 h, 48 h, 72 h).

Results: In AD skin lesions, inflammation- and metabolism-related genes of IDECs are abnormally expressed, and multiple metabolic pathways, including glycolysis/gluconeogenesis, are significantly dysregulated. HDM alone or in combination with SEB activated the glycolysis, induced the upregulation of maturation markers (CD80/83/86) of moIDECs in vitro, and promoted the production of inflammatory cytokines (IL-1β, IL-6, IL-23, IL-10, IL-12 and TNF-α), whereas SEB alone showed no significant effect. Furthermore, we found that HDM dynamically regulated inflammatory immune response of moIDECs. In the early phase (6–24 h), a pro-inflammatory profile predominated, observed with peak levels of IL-6, IFN-γ, IL-18, IL-12, TNF-α and IL-23. This subsequently transitions into the late phase (48–72 h) characterized by an anti-inflammatory shift, marked by elevated IL-10, classical tolerogenic molecules (IDO1, PDL1, and ILT3), and a profile consistent with the potential to induce regulatory T cells (Tregs). Concurrently, metabolic adaptations were observed, with glycolysis peaking at 24 h.

Conclusion: HDM-driven AD progression is correlated with changes in glucose metabolism and a biphasic immune shift in IDECs. Targeting HDM-responsive metabolic pathways like glycolysis might offer novel therapeutic strategies.

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Cite

BibTeXRIS
BibTeX
@article{zhao2026house,
  title = {{House dust mite drives biphasic immunomodulation of inflammatory dendritic epidermal cells via glucose metabolism in atopic dermatitis}},
  author = {Ying Zhao and Cuie Gao and Xin Sui and Lan Ge and Huan Wang and Sisi Deng and Qiquan Chen and Lu Liu and Jing Tian and Tong Mu and Li Wang and Zhiqiang Song},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1887390},
  url = {https://doi.org/10.3389/fimmu.2026.1887390},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - House dust mite drives biphasic immunomodulation of inflammatory dendritic epidermal cells via glucose metabolism in atopic dermatitis
AU  - Ying Zhao
AU  - Cuie Gao
AU  - Xin Sui
AU  - Lan Ge
AU  - Huan Wang
AU  - Sisi Deng
AU  - Qiquan Chen
AU  - Lu Liu
AU  - Jing Tian
AU  - Tong Mu
AU  - Li Wang
AU  - Zhiqiang Song
PY  - 2026
DA  - 2026/10/12
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1887390
UR  - https://doi.org/10.3389/fimmu.2026.1887390
AB  - Background: The impact of environmental antigens, specifically house dust mite (HDM) and Staphylococcus aureus enterotoxin B (SEB), on the metabolism of inflammatory dendritic epidermal cells (IDECs) and its role in atopic dermatitis (AD) pathogenesis is poorly understood. This study aimed to characterize IDECs metabolism in AD and study how antigen exposure drives metabolic reprogramming and immune responses.  Methods: We first analyzed the single-cell RNA transcriptome sequencing data to explore metabolic profiles in IDECs from AD patients. Subsequently, we evaluated the effects of HDM alone or in combination with SEB for 24 h on the energy metabolism, maturation and cytokines secretion of monocytes-derived IDECs (moIDECs) in vitro. Finally, we investigated the dynamic changes of functional and glucose metabolism in moIDECs in vitro treated with HDM at different time points (6 h, 24 h, 48 h, 72 h).  Results: In AD skin lesions, inflammation- and metabolism-related genes of IDECs are abnormally expressed, and multiple metabolic pathways, including glycolysis/gluconeogenesis, are significantly dysregulated. HDM alone or in combination with SEB activated the glycolysis, induced the upregulation of maturation markers (CD80/83/86) of moIDECs in vitro, and promoted the production of inflammatory cytokines (IL-1β, IL-6, IL-23, IL-10, IL-12 and TNF-α), whereas SEB alone showed no significant effect. Furthermore, we found that HDM dynamically regulated inflammatory immune response of moIDECs. In the early phase (6–24 h), a pro-inflammatory profile predominated, observed with peak levels of IL-6, IFN-γ, IL-18, IL-12, TNF-α and IL-23. This subsequently transitions into the late phase (48–72 h) characterized by an anti-inflammatory shift, marked by elevated IL-10, classical tolerogenic molecules (IDO1, PDL1, and ILT3), and a profile consistent with the potential to induce regulatory T cells (Tregs). Concurrently, metabolic adaptations were observed, with glycolysis peaking at 24 h.  Conclusion: HDM-driven AD progression is correlated with changes in glucose metabolism and a biphasic immune shift in IDECs. Targeting HDM-responsive metabolic pathways like glycolysis might offer novel therapeutic strategies.
SN  - 1664-3224
ER  -