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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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IgA Immune Complexes Induce Osteoclast-Mediated Bone Resorption.

Annelot C Breedveld1,2, Melissa M J van Gool1,2, Myrthe A M van Delft1,2

  • 1Department of Molecular Cell Biology and Immunology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, Netherlands.

Frontiers in Immunology
|July 19, 2021
PubMed
Summary
This summary is machine-generated.

IgA autoantibodies in rheumatoid arthritis (RA) patients promote bone resorption by immune cells and osteoclasts, potentially worsening disease severity. Targeting IgA interactions may offer a new therapeutic approach for RA.

Keywords:
ACPAIgAautoantibodiesbone resorptionosteoclastrheumatoid arthritis

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Area of Science:

  • Immunology
  • Rheumatology
  • Pathogenesis of Arthritis

Background:

  • Autoantibodies, including IgA, are common in rheumatoid arthritis (RA).
  • While IgA autoantibodies correlate with severe RA, their specific role in disease pathogenesis, particularly in bone resorption, remains unclear.
  • Understanding the function of IgA immune complexes is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the functional impact of IgA immune complexes on osteoclast-mediated bone resorption in rheumatoid arthritis (RA).
  • To explore the role of IgA autoantibodies in activating immune cells and osteoclasts, contributing to RA pathogenesis.

Main Methods:

  • Quantified IgA and IgG isotypes of anti-citrullinated peptide antibody (ACPA), anti-carbamylated protein (anti-CarP) antibody, and rheumatoid factor (RF) in synovial fluid (SF) from RA patients.
  • Stimulated monocytes, neutrophils, and osteoclasts using SF immune complexes or IgA/IgG-coated beads.
  • Assessed neutrophil extracellular trap (NET) release, cytokine secretion (IL-6, IL-8), and bone resorption activity.

Main Results:

  • SF immune complexes enhanced NET formation compared to serum immune complexes.
  • IgA immune complexes stimulated monocytes to release IL-6 and IL-8, correlating with SF ACPA IgA levels.
  • IgA-activated osteoclasts exhibited significantly increased bone resorption and higher IL-6/IL-8 production compared to IgG-activated osteoclasts.
  • Osteoclasts express FcαRI (CD89) and Fc gamma receptors, mediating IgA and IgG responses.

Conclusions:

  • IgA autoantibodies stimulate immune cells and osteoclasts to release IL-6 and IL-8, enhancing osteoclast-driven bone resorption.
  • This mechanism suggests IgA autoantibodies contribute to RA severity.
  • Targeting IgA-FcαRI interactions presents a potential therapeutic strategy for RA patients with IgA autoantibodies.