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Antibody Transfection into Neurons as a Tool to Study Disease Pathogenesis
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Mimicry and autoantibody-mediated neuronal cell signaling in Sydenham chorea

Christine A Kirvan1, Susan E Swedo, Janet S Heuser

  • 1Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

Nature Medicine
|June 24, 2003
PubMed

Insights

Autoimmune responses to Streptococcus pyogenes can cause Sydenham chorea. Antibodies targeting group A streptococcal carbohydrates activate neuronal signaling, revealing a key mechanism in this neurological disorder.

Area of Science:

  • Neuroimmunology
  • Autoimmunity
  • Microbial Pathogenesis

Background:

  • Acute rheumatic fever (ARF) is a postinfectious autoimmune disease.
  • Sydenham chorea (SC) is the primary neurological manifestation of ARF, but its pathogenesis is poorly understood.
  • Molecular mimicry between Streptococcus pyogenes and host tissues is implicated in ARF.

Purpose of the Study:

  • To identify autoantigens and pathogenic mechanisms in Sydenham chorea.
  • To investigate the role of antibodies in SC pathogenesis.
  • To explore the link between group A streptococcal (GAS) infection and neuronal cell signaling in SC.

Main Methods:

  • Analysis of chorea monoclonal antibodies for antigen specificity.
  • Testing antibody reactivity against neuronal cells.
  • Assessing the effect of antibodies and sera on neuronal signaling pathways, specifically calcium/calmodulin-dependent protein (CaM) kinase II activity.

Main Results:

  • Chorea monoclonal antibodies recognized mammalian lysoganglioside and N-acetyl-beta-D-glucosamine (GlcNAc), the dominant GAS carbohydrate epitope.
  • These antibodies targeted human neuronal cell surfaces.
  • Antibody 24.3.1 and sera from active chorea specifically induced CaM kinase II activity, unlike convalescent or non-chorea sera.

Conclusions:

  • Antibody-mediated neuronal cell signaling is implicated in the immunopathogenesis of Sydenham chorea.
  • This finding provides a potential mechanism for SC and offers insights into other antibody-mediated neurological disorders.
  • Identification of specific autoantigens and pathogenic pathways advances understanding of postinfectious autoimmunity.

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