Viewpoint
Molecular mimicry in the MHC: Hidden clues to autoimmunity?

https://doi.org/10.1016/0167-5699(96)80581-0Get rights and content

Abstract

The term ‘molecular mimicry’ has been used to describe a spectrum of antigenic crossreactivities thought to underlie autoimmune disease. For T cell crossreactivities to occur appropriate T cell clone must be available. Here Harold Baum, Huw Davies and Mark Peakman speculate that an important source of self-peptides that govern thymic selection of such clones are MHC molecular themselves.

References (46)

  • K.W. Wucherpfennig et al.

    Cell

    (1995)
  • M.B.A. Oldstone

    Cell

    (1987)
  • A. Ebringer

    Rheum. Dis. Clin. North Am.

    (1992)
  • H. Baum

    Biochim. Biophys. Acta

    (1995)
  • J. Sloan-Lancaster et al.

    Curr. Opin. Immunol.

    (1995)
  • H. Baum et al.

    Trends Biochem. Sci.

    (1993)
  • S. Albani et al.

    Rheum. Dis. Clin. North Am.

    (1992)
  • M. Fielder et al.

    FEBS Lett.

    (1995)
  • H. Baum et al.

    Lancet

    (1995)
  • H. Baum et al.

    Immunol. Today

    (1994)
  • J.A. Todd

    Immunol. Today

    (1990)
  • T. Lohmann et al.

    Lancet

    (1994)
  • P.G. Ashton-Rickardt et al.

    Immunol. Today

    (1994)
  • R. Hall

    Adv. Parasitol.

    (1994)
  • J. Froude et al.

    Curr. Top. Microbiol. Immunol.

    (1989)
  • R.S. Fujinami et al.

    J. Virol.

    (1988)
  • P. Butler et al.

    Biochem. Mol. Biol. Int.

    (1995)
  • A.K. Burroughs et al.

    Nature

    (1992)
  • A.Y. Rudensky et al.

    Nature

    (1991)
  • D.F. Hunt et al.

    Science

    (1992)
  • R.M. Chicz et al.

    J. Exp. Med.

    (1993)
  • S. Shimoda et al.

    J. Exp. Med.

    (1995)
  • F. Oftung et al.

    Infect. Immun.

    (1994)
  • Cited by (91)

    • Characterization of peripheral blood TCR repertoire in patients with ankylosing spondylitis by high-throughput sequencing

      2018, Human Immunology
      Citation Excerpt :

      However, a previous study found that CD4+ T cell responses, rather than CD8+ T cells, were detrimental in peripheral blood of AS patients [21]. In this regard, an another report has proposed that autoantigen peptides derived from the HLA-B27 heavy chain itself could be recognized by autoreactive CD4+ T cells and then induced autoimmunity [22]. Moreover, increased T-cell oligoclonality have been detected in both CD4+ and CD8+ T cell subsets in peripheral blood of AS patients, supporting the hypothesis that antigen-driver T cell responses results in the induction and/or maintenance of AS [23].

    • Sex differences in immune responses: Hormonal effects, antagonistic selection, and evolutionary consequences

      2017, Hormones and Behavior
      Citation Excerpt :

      Such variability in the MHC genes should in theory enable a larger pathogen peptide binding repertoire, meaning that a wider range of pathogens can be eliminated by the immune system. Too low MHC diversity will be selected against because only a narrow range of pathogen peptides can be presented, and too high MHC diversity will also be selected against because this may reduce the repertoire of T-cells or may increase the risk of cross-reactivity with own peptides, which may trigger autoimmunity (Baum et al., 1996; Benoist and Mathis, 1998; Nowak et al., 1992; Woelfing et al., 2009). Several studies have found evidence of an optimal MHC diversity (Kalbe et al., 2009; Kloch et al., 2010; Madsen and Ujvari, 2006; Woelfing et al., 2009).

    • Inflammation in Juvenile Idiopathic Arthritis

      2007, Rheumatic Disease Clinics of North America
      Citation Excerpt :

      Although the association of MHC alleles with autoimmune diseases has been recognized for many years, the specific mechanism underlying the association is still not fully understood. There are several hypotheses regarding the role of specific MHC molecules in the predisposition to JIA [43–48]. A specific MHC molecule presents the self-protein less effectively than non–disease-related MHC.

    • Dynamical properties of autoimmune disease models: Tolerance, flare-up, dormancy

      2007, Journal of Theoretical Biology
      Citation Excerpt :

      The death of these cells will release large amount of self-antigens which can then stimulate potent immune responses against these self-proteins, leading to strong autoimmunity. Furthermore, virus-induced cross-reactive immune cells can also become the key effector cells (Baum et al., 1996; Horwitz and Sarvetnick, 1999; von Herrath and Oldstone, 1995, 1996). In this way, virus infection has long been associated with the exacerbation of autoimmune disease (however, there is also evidence that viruses can actually protect against autoimmune disease Fujinami, 2001).

    • Inflammation in juvenile idiopathic arthritis

      2005, Pediatric Clinics of North America
    View all citing articles on Scopus
    View full text