Pathogenesis of Polymyalgia Rheumatica

What is the etiopathogenesis of PMR?

The cause of Polymyalgia Rheumatica is unknown. Clues to the diagnosis are provided by the epidemiology of the disease. The higher prevalence in certain populations has suggested a genetic predisposition; an association with HLA-DR4 has been reported. One animal model suggests that both PMR and GCA start with the activation of dendritic cells at the adventitia-media border of the large vessels resulting in the production of IL-1 and IL-6 causing suppression of T-regulatory cells and an increased Th17 response. Unlike GCA, patients with PMR do not recruit T cells capable of producing interferon-γ (IFN-γ). Without IFN-γ to stimulate macrophages, the arterial inflammation characteristic of GCA does not develop. Interestingly, a PMR-like illness has occurred in patients receiving immune checkpoint inhibitors for cancer treatment.

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