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TRIM11 attenuates Treg cell differentiation by p62-selective autophagic degradation of AIM2

Ting Yu1, Xiaofang Yang2, Qiang Fu3

  • 1The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, China; Department of Pharmacy, Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China.

Cell Reports
|October 7, 2023
PubMed

Insights

Tripartite motif-containing motif 11 (TRIM11) negatively regulates regulatory T (Treg) cell differentiation and promotes autoimmune disease by degrading absent in melanoma 2 (AIM2). Targeting TRIM11 may offer new treatments for autoimmune disorders.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Ubiquitination is a key protein modification regulating CD4+ T cell differentiation and function.
  • The roles of most E3 ubiquitin ligases in CD4+ T cell differentiation and related pathologies are not fully understood.

Purpose of the Study:

  • To investigate the function of tripartite motif-containing motif 11 (TRIM11) in CD4+ T cell differentiation and autoimmune disease.
  • To elucidate the mechanism by which TRIM11 influences regulatory T (Treg) cell stability.

Main Methods:

  • Investigated TRIM11's role in CD4+ T cell differentiation and experimental autoimmune encephalomyelitis (EAE) models.
  • Utilized co-immunoprecipitation and Western blotting to study TRIM11-AIM2 interactions and AIM2 degradation.
  • Assessed the impact of AIM2 on signaling pathways (AKT, FOXO1, MYC) and glycolysis in Treg cells.

Main Results:

  • TRIM11 was identified as a negative regulator of Treg cell differentiation in CD4+ T cells.
  • TRIM11 promotes autoimmune disease development through an absent in melanoma 2 (AIM2)-dependent pathway.
  • TRIM11 induces ubiquitination and autophagic degradation of AIM2 via p62, destabilizing Treg cells.
  • AIM2 normally attenuates AKT/FOXO1 phosphorylation, MYC signaling, and glycolysis, promoting Treg stability.

Conclusions:

  • TRIM11 negatively regulates Treg cell differentiation and stability by targeting AIM2 for degradation.
  • TRIM11 plays a crucial role in promoting autoimmune disease pathogenesis.
  • TRIM11 represents a potential therapeutic target for treating autoimmune diseases and cancers driven by immune dysregulation.
Keywords:
CP: ImmunologyTreg cell differentiationprotein post-translational modificationselective autophagic degradation

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