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AIRE expression controls the peripheral selection of autoreactive B cells.

Joel Sng1, Burcu Ayoglu2, Jeff W Chen1

  • 1Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06511, USA.

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|April 14, 2019
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Autoimmune regulator (AIRE) mutations impair central T cell tolerance, leading to autoreactive B cells. AIRE normally prevents these B cells from attacking self-antigens like insulin and cytokines.

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Area of Science:

  • Immunology
  • Endocrinology
  • Genetics

Background:

  • Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome arises from Autoimmune Regulator (AIRE) mutations.
  • AIRE is crucial for central T cell tolerance, preventing autoimmune diseases.

Purpose of the Study:

  • To investigate the role of AIRE and T cells in the peripheral accumulation of autoreactive B cells.
  • To identify self-antigens recognized by autoreactive B cells in AIRE-deficient individuals.

Main Methods:

  • Analysis of CD3- and AIRE-deficient patients.
  • Proteomic arrays and Biacore affinity measurements.
  • T cell receptor (TCR) repertoire analysis in regulatory T cells (Tregs).

Main Results:

  • Lack of T cells or AIRE function caused peripheral accumulation of autoreactive mature naive B cells.
  • These B cells produced antibodies recognizing AIRE-dependent antigens like insulin, IL-17A, and IL-17F.
  • AIRE-deficient patients showed reduced Treg frequencies with a restricted TCR repertoire.

Conclusions:

  • AIRE-mediated T cell and Treg selection is essential for preventing the expansion of autoreactive naive B cells.
  • Defects in AIRE lead to autoimmunity by allowing autoreactive B cells to target self-antigens presented in the thymus.