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TREM2 defends the liver against alveolar echinococcosis by driving fibrous shell formation

Meiling Wang1, Hanrui Guo2, Caiya Ni3

  • 1Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, Shihezi, Xinjiang, China; NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, Shihezi University, Shihezi, Xinjiang, China; Department of Pathology, Jinan Maternity and Child Care Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.

Biochemical Pharmacology
|July 10, 2026
PubMed

Insights

Triggering TREM2 (T-cell immunoglobulin and mucin-domain containing-3) signaling enhances protective fibrosis in alveolar echinococcosis (AE). This TREM2 pathway activation offers a potential therapeutic strategy for AE, a parasitic disease.

Area of Science:

  • Immunology
  • Parasitology
  • Fibrosis Research

Background:

  • Alveolar echinococcosis (AE), caused by E. multilocularis, is characterized by immunosuppression and significant fibrosis.
  • The role of TREM2 (T-cell immunoglobulin and mucin-domain containing-3) in AE pathogenesis, particularly in fibrosis and immune response, is not well understood.

Purpose of the Study:

  • To investigate the function and mechanism of TREM2 in AE.
  • To explore TREM2's role in macrophage behavior and fibrosis formation around E. multilocularis lesions.
  • To identify potential therapeutic targets for AE based on TREM2 signaling.

Main Methods:

  • Immunostaining of human and mouse AE lesions to assess TREM2 expression.
  • Establishment of E. multilocularis infection models in wild-type and Trem2 knockout mice.
  • RNA sequencing, ATAC sequencing, and in vitro assays to analyze TREM2+ macrophage function.
  • In vivo drug screening targeting TREM2 and TGF-β signaling pathways.

Main Results:

  • TREM2+ macrophages were found at the borders of AE lesions in humans and mice.
  • TREM2 deficiency worsened parasitic burden and weakened lesion fibrosis, while TREM2 overexpression enhanced fibrosis.
  • E. multilocularis vesicle fluid induced TREM2 expression via TGF-β/Smad signaling, promoting macrophage migration and fibroblast proliferation.
  • Resiquimod promoted fibrosis, while SB431542 (TGF-β inhibitor) reduced it.

Conclusions:

  • TREM2-mediated fibrosis formation plays a crucial protective role in AE.
  • Targeting TREM2 signaling presents a promising therapeutic strategy for alveolar echinococcosis.
Keywords:
Echinococcus multilocularisFibrous shellResiquimodTGF-β/SmadTREM2

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