Background <p>Rheumatoid arthritis (RA) and giant cell arteritis (GCA) are systemic autoimmune diseases with distinct clinical manifestations that are driven by dysregulation of multiple cell populations of the innate and adaptive immune systems.</p> Objective <p>The aim of this work is to describe and compare the role of central immune cell populations in RA and GCA.</p> Material and methods <p>This review is based on a&#xa0;comprehensive literature search in PubMed. Recent publications on immune cell populations in RA and GCA were assessed for their pathogenic significance and therapeutic implications.</p> Results <p>Both diseases show complex interactions between T&#xa0;cells, B&#xa0;cells, and cells of the innate immune system. A&#xa0;common feature is an imbalance between pro-inflammatory and regulatory mechanisms, ultimately leading to chronic inflammation and tissue damage. Key differences include a&#xa0;dominant role of autoreactive lymphocytes and autoantibodies in RA, whereas dendritic cells and T&#xa0;cell-mediated vascular inflammation are the main drivers in GCA.</p> Conclusion <p>A&#xa0;deeper understanding of these immune cell populations enables new treatment strategies and could be particularly relevant for patients who do not adequately respond to current forms of treatment.</p>

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Immunzellpopulationen in der rheumatoiden Arthritis und Riesenzellarteriitis

  • Laurin Braune,
  • Caroline Schmidt

摘要

Background

Rheumatoid arthritis (RA) and giant cell arteritis (GCA) are systemic autoimmune diseases with distinct clinical manifestations that are driven by dysregulation of multiple cell populations of the innate and adaptive immune systems.

Objective

The aim of this work is to describe and compare the role of central immune cell populations in RA and GCA.

Material and methods

This review is based on a comprehensive literature search in PubMed. Recent publications on immune cell populations in RA and GCA were assessed for their pathogenic significance and therapeutic implications.

Results

Both diseases show complex interactions between T cells, B cells, and cells of the innate immune system. A common feature is an imbalance between pro-inflammatory and regulatory mechanisms, ultimately leading to chronic inflammation and tissue damage. Key differences include a dominant role of autoreactive lymphocytes and autoantibodies in RA, whereas dendritic cells and T cell-mediated vascular inflammation are the main drivers in GCA.

Conclusion

A deeper understanding of these immune cell populations enables new treatment strategies and could be particularly relevant for patients who do not adequately respond to current forms of treatment.