Infectious Triggers of T Cell Autoimmunity

Daniel R. Getts*, Meghann Teague Getts, Nicholas J.C. King, Stephen D. Miller

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Autoimmunity is a significant health concern with diseases like type 1 diabetes (T1D) rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and multiple sclerosis (MS) drastically increasing in prevalence. 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, have been 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 the antimicrobial immune response and development of autoimmune disease will be reviewed.

Original languageEnglish (US)
Title of host publicationThe Autoimmune Diseases
Subtitle of host publicationFifth Edition
PublisherElsevier Inc
Pages263-274
Number of pages12
ISBN (Print)9780123849298
DOIs
StatePublished - Dec 2013

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

  • Immunology and Microbiology(all)

Fingerprint Dive into the research topics of 'Infectious Triggers of T Cell Autoimmunity'. Together they form a unique fingerprint.

Cite this