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Immune cell infiltration and activation" refers to the processes by which immune cells (such as T cells, B cells, NK cells, macrophages, and dendritic cells) migrate into tissues—most commonly tumors or sites of infection—and become functionally activated to execute immune responses[1][3][5]. In cancer, the spatial and functional characterization of these infiltrating immune cells defines the tumor immune microenvironment (TIME) and influences prognosis and response to immunotherapy. High infiltration and activation (the so-called "hot" or immune-inflamed phenotype) often correlates with potential immunotherapy benefit, whereas immune-desert and immune-excluded phenotypes are associated with weak responses[1]. Immune infiltration and activation can be quantified through histology, gene expression signatures, and specific biomarkers. While not a molecular target per se, these processes are leveraged in therapeutic strategies that modulate the trafficking or activity of immune cells, such as immune checkpoint inhibitors, cytokine therapies, and agents targeting the tumor stroma[1][5]. This entry describes a functional process influencing disease states and therapeutic outcomes, not a single molecule or canonical drug target.
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