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Dock8 regulates Th2 cell differentiation through ANXA1.

Ju Liu1, Jianing Tang1, Peiyao Jin2

  • 1Department of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan 430030, China.

Fundamental Research
|April 13, 2026
PubMed
Summary
This summary is machine-generated.

Dedicator of Cytokinesis 8 (DOCK8) deficiency impairs T cell balance, leading to elevated Th2 and Tfh cells that drive IgE production in a mouse model of hyper-IgE syndrome.

Keywords:
ANXA1AR-HIESDock8Th2 cellTreg cell

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Area of Science:

  • Immunology
  • Cell Biology
  • Genetics

Background:

  • Dedicator of Cytokinesis 8 (DOCK8) regulates Rho GTPases (Cdc42, Rac1) crucial for cell migration, adhesion, and phagocytosis.
  • Mutations in DOCK8 cause autosomal recessive hyper-IgE syndrome (AR-HIES), a primary immunodeficiency marked by high IgE, eczema, and infections.

Purpose of the Study:

  • To investigate the immunological effects of DOCK8 deficiency using a CRISPR/Cas9-generated mouse model.
  • To elucidate the role of DOCK8 in T cell homeostasis and its connection to IgE production in AR-HIES.

Main Methods:

  • Generated a CRISPR/Cas9-based mouse model with a Dock81281&1282 TG deletion mutation.
  • Analyzed T cell populations (Tfh, Th2, Treg) and IgE levels in wild-type and mutant mice.

Main Results:

  • DOCK8 is essential for the peripheral homeostasis of T cells, including T follicular helper (Tfh), Th2, and regulatory T cells (Treg).
  • Dock8 mutant mice exhibited elevated Th2 and Tfh cells, which collaboratively promote IgE production.
  • Annexin A1 (ANXA1) was identified to enhance Th2 cell differentiation in Dock8 mutants.

Conclusions:

  • DOCK8 deficiency disrupts T cell balance, contributing to the pathogenesis of AR-HIES.
  • Elevated Th2 and Tfh cells play a key role in the hyper-IgE phenotype.
  • ANXA1 may represent a therapeutic target for restoring immune balance in DOCK8-related disorders.