Molecular mimicry mediated by MHC class lb molecules after infection with gram-negative pathogens

Wei Feng Lo, Amina S. Woods, Amy Decloux, Robert J. Cotter, Eleanor S. Metcalf, Mark J. Soloski

Research output: Contribution to journalArticlepeer-review

Abstract

The development of many autoimmune diseases has been etiologically linked to exposure to infectious agents. For example, a subset of patients with a history of Salmonella infection develop reactive arthritis. The persistence of bacterial antigen in arthritic tissue and the isolation of Salmonella or Yersinia reactive CD8+ T cells from the joints of patients with reactive arthritis support the etiological link between Gram-negative bacterial infection and autoimmune disease. Models proposed to account for the link between infection and autoimmunity include inflammation-induced presentation of cryptic self-epitopes, antigen persistence and molecular mimicry. Several studies support molecular mimicry as a mechanism for the involvement of class II epitopes in infectious disease-induced self- reactivity. Here, we have identified an immunodominant epitope derived from the S. typhimurium GroEL molecule. This epitope is presented by the mouse H2- T23-encoded class lb molecule Qa-1 and was recognized by CD8+ cytotoxic T lymphocytes induced after natural infection. S. typhimurium-stimulated cytotoxic T lymphocytes recognizing the GroEL epitope cross-reacted with a peptide derived from mouse heat shock protein 60 and recognized stressed macrophages. Our results indicate involvement of MHC class lb molecules in infection-induced autoimmune recognition and indicate a mechanism for the etiological link between Gram-negative bacterial infection and autoimmunity.

Original languageEnglish (US)
Pages (from-to)215-218
Number of pages4
JournalNature medicine
Volume6
Issue number2
DOIs
StatePublished - Feb 2000

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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