Fig. 3

DC-T cell crosstalk and the PD-L1/PD-1 signalling axis. This figure summarises the PD-L1/PD-1 signalling axis to maintain immune balance by regulating the function of DCs and T cells. Patients with RA exhibit heightened infiltration of immune cells within their joints, accompanied by immune system dysregulation and impaired T cell function. The activation of synovial fibroblasts is directly facilitated by Th17 through the secretion of IL-17 and IL-22, resulting in an exaggerated immune response in RA. Furthermore, Th17 indirectly exacerbates synovitis and bone destruction in RA by promoting the generation of osteoclasts and subsequent bone resorption. However, there exists a functional inhibition between Th17 cells and Treg, and any abnormalities in the quantity or function of Treg can trigger an immune cascade reaction, resulting in the production of inflammatory factors such as IL-1β, IL-6, and TNF-α, which can lead to joint cartilage damage. PD-1 interacts with its ligand PD-L1 to promote the differentiation of naive T cells into Tregs, which in turn inhibit the differentiation of other CD4⁺T subsets. It has a negative regulatory effect on immune response and can avoid spontaneous immune diseases caused by a persistent inflammatory response. Black arrows indicate the promotion of proliferation and differentiation of CD4⁺T cell subtypes. Inhibition arrows in red indicate inhibition of proliferation and differentiation of CD4⁺T cell subtypes