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Antigen-specific responses in autoimmunity and tolerance.

J W Thomas1

  • 1Division of Rheumatology and Clinical Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232-2681, USA. james.thomas@mcmail.vanderbilt.edu

Immunologic Research
|July 11, 2001
PubMed
Summary

Even with active tolerance, the body can develop insulin antibodies. This review explores how these autoantibodies escape tolerance, impacting conditions like type I diabetes.

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Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmunity

Background:

  • Autoantibodies to insulin occur in autoimmune diseases and after insulin administration.
  • Low hormone levels may prevent tolerance induction, a state of clonal ignorance.
  • Existing research suggests the anti-insulin antibody repertoire is tightly regulated.

Purpose of the Study:

  • To review the mechanisms by which anti-insulin B cells escape immune tolerance.
  • To explain how autoantibodies to insulin are sustained despite active tolerance.

Main Methods:

  • Review of existing literature on insulin autoantibodies.
  • Analysis of B cell tolerance induction and regulation.
  • Examination of V gene origins and structure in insulin antibodies.

Main Results:

  • Tolerance to insulin is actively maintained, even for low concentrations.
  • B cells in mice with insulin antibody transgenes are functionally silenced.
  • Insulin antibodies persist due to activation by TI antigen signals, unique epitope display, and cross-reactivity.

Conclusions:

  • Active tolerance mechanisms exist for small molecules like insulin.
  • Specific escape pathways allow anti-insulin B cells to persist in the repertoire.
  • Understanding these pathways is crucial for managing insulin autoimmune syndrome and type I diabetes.

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