Table 1.

Summary of immune response processes to TECs.

Events in Immune Responses after TEC’s Implantation	Role in TEC’s Rejection or Tissue Regeneration
Release of DAMPs	They are released by injured cells, triggering recruitment, proliferation, and activation of non-hematopoietic and hematopoietic cells, culminating in tissue repair. Outcome varies based on immune response duration and cell involvement.
Adsorption of plasma proteins to scaffold’s surface	Biomaterial properties influence protein binding on scaffold surfaces, dictating immune responses. Adsorbed proteins initiate cellular reactions, triggering inflammation and complement activation, contributing to clot formation and inflammation.
Recognition of TEC as a foreign body	Histamine, cytokines, and leukotrienes released by platelets and endothelial cells trigger neutrophil mobilization at TEC implant sites. Resident cells detect DAMPs, releasing IL-8 to attract neutrophils, initiating an inflammatory response.
Recruitment of neutrophils	Neutrophils are recruited at implant site within 72 h to combat infections by producing cytotoxic substances and reactive oxygen species. They also release neutrophil extracellular traps and IL-8, amplifying the inflammatory response and potentially degrading TEC’s surface.
Activation of mast cells	Mast cells sense biomaterial scaffolds, releasing inflammatory substances upon activation, influencing immune cell behavior, notably macrophages.
Macrophages	In the early healing stages, macrophages bind to scaffold proteins and attempt to engulf the biomaterial. The crosstalk between macrophages and neutrophils is particularly crucial for initiating tissue repair. Increased expression of phagocytic signals on the surface of dying neutrophils prompts the activation of macrophages.
Formation of FBGCs	In the chronic phase of the foreign body response, FBGCs form from fused macrophages on the implant surface. Influenced by cytokines and scaffold composition, FBGCs release substances shaping immune responses and biomaterial degradation, impacting implant outcome.
TH2 cell activation	Under IL-4 stimulation, FBGCs adopt a pro-remodeling phenotype, aiding tissue repair by boosting Th2 cell response. This activation enhances IL-4-like cytokine release, fortifying macrophage pro-remodeling traits. These stimulated macrophages, linked to improved scaffold outcomes, collaborate with fibroblasts and stem cells, fostering tissue regeneration and functional implants.