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The inflamed tissue microenvironment and immune cell populations represent a complex, multi-component biological system rather than a single molecular target (1). This environment is composed of various immune cells—such as T cells, macrophages, and neutrophils—interacting with stromal cells and the extracellular matrix (2). It is characterized by distinct physiological conditions, including hypoxia, acidosis, and a high concentration of inflammatory mediators like cytokines and chemokines (3). In diseases such as cancer and chronic autoimmunity, this microenvironment is often reprogrammed to support disease progression or immune evasion (4). While drugs do not target the environment as a whole, many therapeutic agents are designed to modulate specific pathways within it, such as the PD-1/PD-L1 checkpoint or TNF-alpha signaling (5). Understanding the spatial organization and functional states of these immune cell populations is critical for predicting therapeutic efficacy and developing next-generation immunotherapies (6).
Modulation of immune cell recruitment, activation, or suppression; neutralization of pro-inflammatory cytokines; and alteration of the physical-chemical properties of the tissue niche.
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