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Immune and inflammatory cells within the injury site represent a heterogeneous population of leukocytes, including neutrophils, macrophages, and lymphocytes, that migrate to areas of tissue damage or infection (Kumar et al., Robbins Basic Pathology, 2020). These cells are central to the inflammatory response, releasing cytokines and chemokines to coordinate defense and initiate tissue repair (Janeway et al., Immunobiology, 2001). In chronic conditions, persistent activation of these cells can lead to tissue destruction and fibrosis (StatPearls, Inflammation, 2023). While these cells are the focus of many immunomodulatory therapies, they are considered a biological compartment or environment rather than a single molecular target (Nature Reviews Drug Discovery, 2018). Therapeutic strategies often target specific receptors or signaling molecules within these cells, such as TNF-alpha or JAK kinases, to achieve clinical efficacy (NIH, National Institute of Allergy and Infectious Diseases). Consequently, drugs interacting with this population typically aim to suppress overactive immune responses or promote a pro-resolving phenotype in macrophages to restore homeostasis (PubMed, PMCID: PMC7019230).
Drugs modulate these cells by inhibiting specific signaling pathways (e.g., NF-kB), blocking cytokine receptors, or preventing cell recruitment to the site of injury.
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