6533b855fe1ef96bd12afd91

RESEARCH PRODUCT

Pathogenesis of polymyalgia rheumatica

Francesco CicciaGiovanni TrioloFederica MacalusoGiuliana GugginoAngelo Ferrante

subject

musculoskeletal diseaseslcsh:Internal medicineGiant Cell ArteritisAdaptive immunityeducationlcsh:MedicineDiseaseT-Lymphocytes RegulatoryPathogenesisPolymyalgia rheumatica03 medical and health sciences0302 clinical medicineImmune systemRheumatologyPathogenesiHumansMedicinelcsh:RC31-1245Giant Cell ArteritiB cellAgedInnate immunity030203 arthritis & rheumatologyB-LymphocytesEvidence-Based MedicineInnate immune systembusiness.industrylcsh:RPolymyalgia rheumaticaB-LymphocyteCell DifferentiationBiomarkerPathogenesis.medicine.diseaseAcquired immune systemImmunity InnateSettore MED/16 - ReumatologiaGiant cell arteritismedicine.anatomical_structure030220 oncology & carcinogenesisImmunologyTh17 CellsbusinessBiomarkersHuman

description

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.

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