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HLA-DR3 restricted environmental epitopes from the bacterium Clostridium tetani have T cell cross-reactivity to the

Zhenhuan Zhao1,2, Ashley N Anderson2, Carol C Kannapell1,2

  • 1Division of Rheumatology, Department of Medicine, University of Virginia, Charlottesville, VA, United States.

Frontiers in Immunology
|November 17, 2022
PubMed

Insights

A bacterial epitope mimic, ABC247-261, activates T cells and induces autoantibodies in individuals with HLA-DR3, potentially contributing to systemic lupus erythematosus (SLE) development.

Area of Science:

  • Immunology
  • Autoimmunity
  • Molecular Biology

Background:

  • HLA-DR3 (DR3) is a significant genetic factor in systemic lupus erythematosus (SLE) susceptibility.
  • Previous research identified T cell epitopes within the Smith D (SmD) protein restricted by DR3.
  • A library of bacterial epitope mimics was created based on these DR3-restricted epitopes.

Purpose of the Study:

  • To identify novel bacterial T cell epitopes that mimic self-antigens.
  • To investigate the role of a specific bacterial mimic, ABC247-261, in T cell activation and autoantibody production.
  • To compare the autoimmune potential of bacterial mimics versus known Tetanus toxoid (TT) epitopes in DR3 individuals.

Main Methods:

  • Generation of a non-homologous bacterial epitope mimics library.
  • Identification and characterization of the ABC247-261 Mimic from *Clostridium tetani*.
  • In vivo studies assessing T cell activation, autoantibody induction, and cross-reactivity in SLE patients and healthy donors.
  • Analysis of Tetanus toxoid (TT) epitopes for their ability to induce autoimmune T cells.

Main Results:

  • The ABC247-261 Mimic, a DR3-restricted bacterial epitope, activated autoreactive SmD66-80-specific T cells and induced autoantibodies in vivo.
  • SLE patients exhibited a higher percentage of cross-reactive T cells to ABC247-261 Mimic and SmD66-80 compared to healthy donors.
  • The TT epitope TT826-845 stimulated SmD66-80 reactive T cells but did not induce persistent anti-SmD autoantibodies, unlike the ABC247-261 Mimic.

Conclusions:

  • Exposure to the bacterial ABC247-261 Mimic may contribute to the development of autoimmunity in individuals carrying the HLA-DR3 allele.
  • Bacterial epitope mimics can effectively induce autoimmune responses relevant to SLE pathogenesis.
  • Cross-reactivity between bacterial epitopes and self-antigens is a potential mechanism driving autoimmunity in HLA-DR3 positive individuals.
Keywords:
HLA-DR3Smith D (SmD)T cell epitopeautoantigencross-reactive T cellsenvironmental bacteriamolecular mimicrysystemic lupus erythematosus (SLE)

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