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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Host–Microbe Crosstalk in Sjögren’s Disease: Epithelial Type I Interferon Amplification, Loss of Short-Chain Fatty Acid Restraint, and the Effector-Phase Focus of Validated Therapy

  • Minjae Yu1,2,3
  • Dahee Jo2,4
  • Yeonhee Hwang2,4
  • Kyudong Han1,2,3,4,5
5 affiliations
  1. 1Department of Bioconvergence Engineering, Dankook University, Yongin 16890, Republic of Korea
  2. 2Center for Bio-Medical Engineering Core Facility, Dankook University, Cheonan 31116, Republic of Korea
  3. 3Smart Animal Bio Institute, Dankook University, Cheonan 31116, Republic of Korea
  4. 4Department of Microbiology, College of Science & Technology, Dankook University, Cheonan 31116, Republic of Korea
  5. 5Global Chemical Convergence Research Institute, Dankook University, Cheonan 31116, Republic of Korea
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Abstract

Sjögren’s disease (SjD) is a systemic autoimmune disease of the exocrine glands, long framed as a lymphocyte-driven disorder in which immune cells destroy the target tissue. Genomic, epigenetic, microbiome, and single-cell and spatial studies have since shown the glandular epithelium and the microbial environment to be active participants rather than passive bystanders. This review asks whether host susceptibility and microbiome change can be joined into one continuous axis, following it from genetic and epigenetic susceptibility, through microbiome change read functionally rather than taxonomically, to the crosstalk that converts microbial signals into a host response and the cell states carrying it in human tissue. Two axes run through the whole sequence: the type I interferon (IFN) response and short-chain fatty acid (SCFA) metabolism. Read against them, every disease-modifying therapy with validated efficacy so far acts in the downstream B-cell effector axis, whereas the upstream IFN axis has yielded no established treatment. Because the microbial layer and the salivary gland transcriptome or proteome have never been measured in the same patients, the model proposed here remains a testable hypothesis rather than a completed causal chain. The aim is to specify that model, the falsification conditions it carries, and the study design its verification requires.

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Cite

BibTeXRIS
BibTeX
@article{yu2026hostmicrobe,
  title = {{Host–Microbe Crosstalk in Sjögren’s Disease: Epithelial Type I Interferon Amplification, Loss of Short-Chain Fatty Acid Restraint, and the Effector-Phase Focus of Validated Therapy}},
  author = {Minjae Yu and Dahee Jo and Yeonhee Hwang and Kyudong Han},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209042},
  url = {https://www.mdpi.com/1422-0067/27/20/9042},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Host–Microbe Crosstalk in Sjögren’s Disease: Epithelial Type I Interferon Amplification, Loss of Short-Chain Fatty Acid Restraint, and the Effector-Phase Focus of Validated Therapy
AU  - Minjae Yu
AU  - Dahee Jo
AU  - Yeonhee Hwang
AU  - Kyudong Han
PY  - 2026
DA  - 2026/10/12
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209042
UR  - https://www.mdpi.com/1422-0067/27/20/9042
AB  - Sjögren’s disease (SjD) is a systemic autoimmune disease of the exocrine glands, long framed as a lymphocyte-driven disorder in which immune cells destroy the target tissue. Genomic, epigenetic, microbiome, and single-cell and spatial studies have since shown the glandular epithelium and the microbial environment to be active participants rather than passive bystanders. This review asks whether host susceptibility and microbiome change can be joined into one continuous axis, following it from genetic and epigenetic susceptibility, through microbiome change read functionally rather than taxonomically, to the crosstalk that converts microbial signals into a host response and the cell states carrying it in human tissue. Two axes run through the whole sequence: the type I interferon (IFN) response and short-chain fatty acid (SCFA) metabolism. Read against them, every disease-modifying therapy with validated efficacy so far acts in the downstream B-cell effector axis, whereas the upstream IFN axis has yielded no established treatment. Because the microbial layer and the salivary gland transcriptome or proteome have never been measured in the same patients, the model proposed here remains a testable hypothesis rather than a completed causal chain. The aim is to specify that model, the falsification conditions it carries, and the study design its verification requires.
SN  - 1422-0067
ER  -