Current Insights into Tissue Injury of Giant Cell Arteritis: From Acute Inflammatory Responses towards Inappropriate
Dimitris Anastasios Palamidas1, Loukas Chatzis1,2, Maria Papadaki2
1Department of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Cells
|March 13, 2024
Summary
Giant cell arteritis (GCA) involves inflammation of large arteries, primarily affecting individuals over 50. This review details GCA pathogenesis, highlighting key cells and molecules in its inflammatory phases.
Area of Science:
- Immunology
- Rheumatology
- Pathology
Background:
- Giant cell arteritis (GCA) is an autoimmune disease impacting large vessels in patients >50 years old.
- Interleukin-6 (IL-6) is central to GCA's inflammatory processes.
- Comorbidities include blindness from vascular occlusion and thoracic aorta aneurysms.
Purpose of the Study:
- To review current advances in understanding GCA pathogenesis.
- To describe cells, molecules, and mediators involved in GCA's inflammatory phases.
Main Methods:
- Review of current literature on GCA pathogenesis.
- Analysis of cellular and molecular mechanisms in different inflammatory phases.
Main Results:
- GCA involves monocytes/macrophages, Th1/Th17 responses, B-cells, and neutrophils.
- Senescent cells and neutrophil extracellular traps are found in GCA lesions.
- Understanding early disease stages and cell interactions remains challenging.
Conclusions:
- GCA pathogenesis involves complex, overlapping inflammatory phases.
- Further research is needed to elucidate early disease mechanisms and cell interactions.
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