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Pathological autoantibody internalisation in myositis.

Iago Pinal-Fernandez1,2, Sandra Muñoz-Braceras3, Maria Casal-Dominguez3,2

  • 1Muscle Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA andrew.mammen@nih.gov iago.pinalfernandez@nih.gov.

Annals of the Rheumatic Diseases
|June 20, 2024
PubMed
Summary
This summary is machine-generated.

In myositis, autoantibodies enter muscle cells and disrupt their function, challenging previous assumptions. This finding has implications for understanding autoimmune myopathies and developing targeted therapies.

Keywords:
AntibodiesAutoantibodiesDermatomyositisPolymyositis

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Area of Science:

  • Immunology
  • Molecular Biology
  • Muscle Biology

Background:

  • Autoantibodies targeting intracellular proteins are prevalent in autoimmune diseases.
  • The role of these autoantibodies in myositis has been debated due to the belief that they cannot penetrate muscle cells.

Purpose of the Study:

  • To investigate whether autoantibodies can enter living muscle cells in myositis.
  • To determine if internalised autoantibodies cause functional changes in muscle cells.

Main Methods:

  • Confocal immunofluorescence microscopy to localize antibodies in muscle biopsies.
  • Bulk RNA sequencing of 669 muscle samples (myositis, controls).
  • Electroporation of patient antibodies into cultured myoblasts followed by RNA sequencing.

Main Results:

  • Myositis autoantibodies were found within muscle fibers, co-localizing with their autoantigens.
  • Muscle biopsies with autoantibodies targeting transcriptional regulators showed transcriptomic changes indicating autoantigen dysfunction.
  • Specific examples include altered RNA processing in patients with anti-PM/Scl antibodies.
  • In vitro experiments confirmed that patient antibodies induce similar transcriptomic changes in muscle cells.

Conclusions:

  • Autoantibodies are internalized into living muscle cells in myositis.
  • Internalized autoantibodies disrupt the function of their target autoantigens, leading to observable biological effects.