Macrophages in polymyalgia rheumatica
Macrophages in polymyalgia rheumatica
Polymyalgia rheumatica (PMR) is an inflammatory disease that commonly affects people over the age of 50. It causes severe pain and stiffness in the shoulders and hips. The inflammation is mainly located in structures surrounding the joints, such as bursae. In contrast to other rheumatic diseases, little is known about the underlying inflammatory processes in PMR. As a result, treatment options remain limited. This thesis of Anqi Zhang investigates the role of an important type of immune cell, the macrophage, in the pathogenesis of PMR.
Macrophages develop from monocytes, immune cells that circulate in the bloodstream. Patients with PMR were found to have increased numbers of monocytes in their blood. In inflamed bursal tissue, these monocytes differentiate into highly activated macrophages that produce large amounts of inflammatory proteins, including interleukin-6 (IL-6).
Macrophage activation in PMR is stimulated by other inflammatory proteins, such as GM-CSF and interferon-γ, produced by T cells. In addition, macrophages produce galectin-3, which stimulates connective tissue cells (fibroblasts) to generate more inflammatory proteins and attract additional immune cells. This interaction helps sustain the inflammatory process.
Because PMR frequently occurs together with giant cell arteritis (GCA), an inflammatory disease of the blood vessels, similarities between the two conditions were also examined. The shared immune features in affected bursal and vascular tissues support the concept that PMR and GCA are part of a single disease spectrum.
Overall, the research described in this thesis demonstrates that macrophages play a central role in the development and persistence of PMR and identifies potential targets for more effective, tailored therapies.