https://doi.org/10.4081/reumatismo.2018.1048

Pathogenesis of polymyalgia rheumatica

Vol. 70 No. 1 (2018): Monographic issue on Polymyalgia Rheumatica
Submitted: 21 July 2017
Accepted: 18 January 2018
Published: 27 March 2018
Polymyalgia rheumatica, Innate immunity, Adaptive immunity, Pathogenesis.
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Authors

G. Guggino
Biomedical Department of Internal Medicine, Division of Rheumatology, University of Palermo, Italy.
A. Ferrante
Biomedical Department of Internal Medicine, Division of Rheumatology, University of Palermo, Italy.
F. Macaluso
Biomedical Department of Internal Medicine, Division of Rheumatology, University of Palermo, Italy.
G. Triolo
Biomedical Department of Internal Medicine, Division of Rheumatology, University of Palermo, Italy.
F. Ciccia
francesco.ciccia@unipa.it
Biomedical Department of Internal Medicine, Division of Rheumatology, University of Palermo, Italy.
Polymyalgia rheumatica (PMR) is a chronic, inflammatory disorder of unknown cause, almost exclusively occurring in people aged over 50 and often associated with giant cell arteritis. The evidence that PMR occurs almost exclusively in individuals aged over 50 may indicate that age-related immune alterations in genetically predisposed subjects contribute to development of the disease. Several infectious agents have been investigated as possible triggers of PMR even though the results are inconclusive. Activation of the innate and adaptive immune systems has been proved in PMR patients as demonstrated by the activation of dendritic cells and monocytes/macrophages and the altered balance between Th17 and Treg cells. Disturbed B cell distribution and function have been also demonstrated in PMR patients suggesting a pathogenesis more complex than previously imagined. In this review we will discuss the recent findings regarding the pathogenesis of PMR.

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How to Cite

Guggino, G., Ferrante, A., Macaluso, F., Triolo, G., & Ciccia, F. (2018). Pathogenesis of polymyalgia rheumatica. Reumatismo, 70(1), 10–17. https://doi.org/10.4081/reumatismo.2018.1048

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