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The foreign body response is a stereotyped tissue reaction to the implantation of foreign materials (such as medical devices) in the body. It begins with protein adsorption to the implant surface, recruitment of neutrophils and macrophages, fusion of macrophages into multinucleated foreign body giant cells, and progressive activation of fibroblasts and formation of a fibrotic capsule that can isolate the device. This process is driven by both innate and adaptive immune signals, cytokines (e.g., IL-4, IL-13), adhesion molecules, and biomechanical factors. The resulting tissue response determines the biocompatibility, durability, and therapeutic function of medical implants, and excessive foreign body response may lead to chronic inflammation, pain, device failure, or encapsulation. While highly clinically relevant, "foreign body response" is a process involving multiple cell types and molecular signals rather than a druggable molecular target. It cannot be directly targeted as a receptor, enzyme, or protein; instead, therapeutic strategies aim to modulate the various steps and cell mediators that contribute to the pathological aspects of the response.
Drugs target components of the response such as: Inhibition of inflammatory cytokine signaling; Blockade of immune cell recruitment/adhesion; Reduction of fibroblast activation and fibrosis; Modification of protein adsorption on biomaterials.
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