Microbial infection as a trigger of t-cell autoimmunity

Daniel R. Getts, Alanna Spiteri, Nicholas J.C. King, Stephen D. Miller

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

Abstract

Autoimmunity is a significant health concern with diseases such as type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis, drastically increasing in prevalence over the last 30-40 years. The precise trigger for autoimmunity is unknown, although genetics clearly plays a significant role. However, low concordance rates in monozygotic twins as well as geographical distribution patterns suggest that the development of autoimmunity is the culmination of multiple factors, with genetic predisposition being only one component. Retrospective epidemiological and animal studies have shown that infection is an important factor in the generation of autoimmune disease. Traditionally, cross-reactive T-cell recognition, known as molecular mimicry, as well as bystander T-cell activation culminating in epitope spreading are considered the predominant mechanisms through which infection may culminate in an autoimmune response. Notwithstanding, recent studies suggest other avenues, including microbial toxins and virus-induced decoy of the immune system, may also play a role. In this chapter, the relationship between antimicrobial immune responses and development of autoimmune disease will be reviewed.

Original languageEnglish (US)
Title of host publicationThe Autoimmune Diseases
PublisherElsevier
Pages363-374
Number of pages12
ISBN (Electronic)9780128121023
ISBN (Print)9780128122426
DOIs
StatePublished - Jan 1 2019

Keywords

  • Autoimmune disease
  • Bystander activation
  • Epitope spreading
  • Microbial superantigens
  • Molecular mimicry
  • Pathogen-associated molecular patterns
  • Pattern recognition receptors
  • T-cell receptor affinity

ASJC Scopus subject areas

  • Medicine(all)
  • Immunology and Microbiology(all)

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