Effects of immune cells on mesenchymal stem cells during fracture healing

Figure 7 Schematic overview of the regulatory role of B-cells during fracture healing. Fracture healing is affected by interactions between mesenchymal stem cells (MSCs) and B-cells. MSCs may affect B-cells by factors, e.g., interleukin 2 (IL-2), prostaglandin E2, and interferon gamma (IFN-γ), which interact with the programmed cell death 1 receptor and its ligand. Resulting in activation of mitogen-activated protein kinase and its downstream target MEK partner 1, induces B-cells to secrete/release factors, e.g., tumor necrosis factor alpha, transforming growth factor beta, IL-10, and C-C-motif chemokine ligand 3. Colored arrows depict stimulation and blunt end lines inhibition. Dashed black arrows indicate differentiation processes. CD: Cluster of differentiation; TNF-α: Tumor necrosis factor alpha; IL: Interleukin; IFN: Interferon; CCL: C-C-motif chemokine ligand; TGF-β: Transforming growth factor beta; PGE2: Prostaglandin E2; Tregs: Regulatory T cells; MAPK: Mitogen-activated protein kinase; PD-1: Programmed cell death 1; PD-L1: Programmed cell death ligand 1; MP1: MEK partner 1.