Synovial Macrophages: Past Life, Current Situation, and Application in Inflammatory Arthritis

Abstract

Inflammatory arthritis is an inflammatory disease that involves the joints and surrounding tissues. Synovial hyperplasia often presents when joints become inflamed due to immune cell infiltration. Synovial membrane is an important as well as a highly specific component of the joint, and its lesions can lead to degeneration of the joint surface, causing pain and joint disability or affecting the patients’ quality of life in severe cases. Synovial macrophages (SMs) are one of the cellular components of the synovial membrane, which not only retain the function of macrophages to engulf foreign bodies in the joint cavity, but also interact with synovial fibroblasts (SFs), T cells, B cells, and other inflammatory cells to promote the production of a variety of pro-inflammatory cytokines and chemokines, such as TNF-α, IL-1β, IL-8, and IL-6, which are involved in the pathogenic process of inflammatory arthritis. SMs from different tissue sources have differently differentiated potentials and functional expressions. This article provides a summary on studies pertaining to SMs in inflammatory arthritis, and explores their role in its treatment, in order to highlight novel treatment modalities for the disease.

PFS alleviates bone destruction in collagen-induced arthritis mice associated with macrophage polarization

“…TNF and IL-1 are important drivers of bone and cartilage damage in RA [25, 26]. M2 macrophages promote angiogenesis, tissue remodeling, and repair by producing high levels of anti-inflammatory factors including IL-10, TGF-β, and Arg1[6, 27]. Macrophages can also directly differentiate into mature osteoclasts influenced by the inflammatory environment, further exacerbating bone erosion [28, 29].…”

Advancement in understanding the role of ferroptosis in rheumatoid arthritis

“…Rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) lead to the proliferation of synovial membrane, inflammatory reactions, extensive angiogenesis, the disintegration of cartilage matrix, and destruction of bones by producing abundant pro-inflammatory cytokines and chemokines ( Bartok and Firestein, 2010 ; Aldridge et al, 2020 ; Bai et al, 2022 ; Ji et al, 2022 ); Figure 1 ). RA-FLS continuously produces many inflammatory factors like IL-6, IL-1β, TNF-α, vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs).…”