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Selected Publication:
SHR Neuro Cancer Cardio Lipid Metab Microb
Dejaco, C; Wagner, AD.
Aetiology and Pathogenesis of Polymyalgia Rheumatica and Giant-cell Arteritis
AKTUEL RHEUMATOL. 2014; 39(4): 256-260.
Doi: 10.1055/s-0034-1333661
Web of Science
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- Leading authors Med Uni Graz
- Dejaco Christian
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- Abstract:
- Polymyalgia rheumatica (PMR) and giant-cell arteritis (GCA) are closely related conditions with unclear aetiology. Genetic factors including female sex and polymorphisms in the HLA II gene, adhesion molecules and chemokines, as well as infections may play important roles in the pathogenesis of the disease. Serological and tissue analyses for viral and bacterial agents (including Parvovirus B19 and Chlamydia pneumoniae), however, revealed conflicting results. Age-related changes of the immune and vascular system with the accumulation of pro-inflammatory cytokines and oxidative end-products as well as abnormalities in the endocrine axes (e.g., inadequate low endogenous cortisol production, loss of androgens) may all together contribute to the disease process. In GCA but not in PMR, abnormal maturation of dendritic cells leads to the recruitment of IFN-gamma producing CD4+ T-cells and macrophages into the vessel wall. Macrophages produce matrix metalloproteinases causing a destruction of small muscle cells and the internal elastic membrane. They also release growth factors including platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) leading to intima hyperplasia and vascular occlusion.
- Find related publications in this database (Keywords)
- polymyalgia rheumatica
- giant cell arteritis
- T-cells
- etiology