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Growth Arrest-Specific 6 Enhances the Suppressive Function of CD4+CD25+ Regulatory T Cells Mainly through Axl

Guang-Ju Zhao1, Jia-Yi Zheng2, Jia-Lan Bian1

  • 1Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.

Mediators of Inflammation
|March 9, 2017
PubMed

Insights

Growth arrest-specific 6 (Gas6) enhances the function of regulatory T cells (Tregs), which are crucial for preventing autoimmunity. Gas6 primarily acts through the Axl receptor to boost Treg suppressive activity.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Growth arrest-specific 6 (Gas6) is an endogenous ligand for TAM receptors (Tyro3, Axl, Mertk) with known immune-modulating roles.
  • CD4+CD25+ regulatory T cells (Tregs) are vital for suppressing autoimmune responses.

Purpose of the Study:

  • To investigate TAM receptor expression on Tregs.
  • To determine the role of the Gas6-TAM signaling pathway in regulating Treg suppressive function.

Main Methods:

  • Assessed TAM receptor (Axl, Mertk) expression on Tregs using Western blot, immunofluorescence, flow cytometry, and RT-PCR.
  • Investigated Gas6's effect on Treg suppressive function via CFSE-based proliferation assays, flow cytometry for Foxp3/CTLA-4, and ELISA for cytokine secretion.
  • Utilized siRNA and antibodies to silence or block TAM receptors.

Main Results:

  • Tregs express both Axl and Mertk receptors.
  • Gas6 significantly enhances Treg suppressive function both in vitro and in vivo.
  • Gas6 stimulation upregulates Foxp3 and CTLA-4 expression on Tregs.
  • Gas6's enhancement of Treg suppressive activity is predominantly mediated through the Axl receptor.

Conclusions:

  • Gas6 directly influences the function of CD4+CD25+ Tregs.
  • The interaction between Gas6 and the Axl receptor is key to modulating Treg suppressive activity.

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