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A divergent population of autoantigen-responsive CD4+ T cells in infants prior to β cell autoimmunity

Anne-Kristin Heninger1, Anne Eugster1, Denise Kuehn1

  • 1DFG-Center for Regenerative Therapies Dresden, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Fetscherstraße 105, 01307 Dresden, Germany.

Science Translational Medicine
|February 24, 2017
PubMed

Insights

Early immune signatures in children predict autoimmune diabetes. Naïve CD4+ T cells show distinct gene expression in infancy, preceding autoantibodies and guiding future prevention strategies for type 1 diabetes.

Area of Science:

  • Immunology
  • Endocrinology
  • Genetics

Background:

  • Autoimmune diabetes arises from immune system sensitization to pancreatic beta cell antigens during childhood.
  • Early identification of at-risk individuals is crucial for intervention and prevention strategies.

Purpose of the Study:

  • To identify early molecular signatures in T cells that predict the development of autoimmune diabetes in at-risk children.
  • To understand the longitudinal changes in T cell populations from infancy through the development of autoimmunity.

Main Methods:

  • Longitudinal follow-up of at-risk infants.
  • Single-cell gene expression analysis of beta cell antigen-responsive CD4+ T cells.
  • Monitoring for the emergence of autoantibodies and clinical autoimmunity.

Main Results:

  • A distinct gene expression signature in naive CD4+ T cells was observed in infancy among children who later developed autoimmune diabetes, predating memory T cell or autoantibody formation.
  • This early signature indicated a pre-T helper 1 (TH1)/TH17/T follicular helper cell profile.
  • Upon autoantibody emergence, these cells transitioned to an interferon-gamma (IFNG)-producing TH1 memory phenotype.

Conclusions:

  • The identified naive T cell gene signature in infancy serves as an early biomarker for autoimmune diabetes risk.
  • Perinatal exposures may influence this divergent T cell response, suggesting potential targets for prevention.
  • This discovery can inform future diagnostic and preventative approaches for beta cell autoimmunity.

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