Abstract
The ontogeny of macrophages in most organs has already been established. Owing to the limited number and inaccessibility of synovial macrophages (SMs), the origin of SMs has not been fully elucidated. Previous studies suggested that SMs have two major origins, namely, tissue-resident and monocyte-derived SMs. However, no systematic analysis to identify SM ontology in either physiological or pathological conditions has been available to date. In this review, we summarize relevant studies on the two main origins of SMs in rheumatoid arthritis (RA) and forecast the future research directions for this field. Furthermore, we discuss the current state of RA therapy that is based on targeting different SM subsets.
Highlights
We summarize relevant studies on the two main origins of synovial macrophages (SMs) in rheumatoid arthritis (RA) and forecast the future research directions for this field
Macrophages produce various cytokines and chemokines, and they are involved in cartilage and bone destruction, which can critically contribute to the pathogenesis of RA [3]
The healthy joint synovium is a thin piece of tissue that only contains a few layers of cells
Summary
In 1967, Takasugi and Hollingsworth found a group of large, phagocytic cells (macrophage-like cells) in fluids from rheumatoid arthritis (RA) patients [1]. CD14+ cells showed a phenotype characteristic of circulating monocytes rather than tissue-resident SMs, characterized by high expression of CCR2, MRP8, and MRP14, but low expression of MERTK and 25F9 These cells had the capacity to produce proinflammatory cytokines. SM (CD14+ and CD68+) depletion by clodronate-containing liposome injections can decrease expression of adhesion molecules (VCAM-1 and ICAM-1) in the lining layer of RA patients [24] These methods are all designed to target total SMs without discriminating the different subsets of SMs. As suggested in a previous study [21], F4/80+ resident murine SMs show anti-inflammatory phenotype. This study suggested that the treatment influenced the immunoregulation of rat SMs [27]
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