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IgLON5-IgG: Innocent Bystander or Perpetrator?

Jane Andersen1,2, Bronte Jeffrey1,3, Winny Varikatt2,4

  • 1Department of Immunology, NSW Health Pathology-ICPMR, Westmead Hospital, Sydney, NSW 2145, Australia.

International Journal of Molecular Sciences
|July 27, 2024
PubMed
Summary

Anti-IgLON5-associated disease pathogenesis is debated, with evidence supporting both neurodegenerative and autoimmune mechanisms. Multiple immune pathways likely contribute to this rare neurological condition.

Keywords:
IgLON5IgLON5-IgGanti-IgLON5-associated diseaseautoimmune encephalitisneurodegeneration

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Area of Science:

  • Neurology
  • Immunology
  • Neuroimmunology

Background:

  • Anti-IgLON5 (IgLON5-IgG)-associated disease is a recently identified clinical entity.
  • Its underlying pathogenesis remains incompletely understood, necessitating further investigation.

Purpose of the Study:

  • To review and evaluate the evidence for different pathogenetic mechanisms in Anti-IgLON5-associated disease.
  • To explore the potential roles of neurodegeneration and autoimmunity in disease development.

Main Methods:

  • Literature review of existing studies on Anti-IgLON5-associated disease.
  • Analysis of neuropathological findings, genetic associations, and immunological markers.

Main Results:

  • Evidence for neurodegeneration includes tauopathy and MAPT H1/H1 genotype.
  • Evidence for autoimmunity includes IgLON5 cell-surface localization, antibody pathogenicity, HLA associations (DRB1*10:01, DQB1*05:01), and immunotherapy response.

Conclusions:

  • The pathogenesis of Anti-IgLON5-associated disease is likely multifactorial, involving both neurodegenerative and autoimmune processes.
  • Heterogeneity in disease presentation suggests diverse immune mechanisms may operate simultaneously.