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Pro-inflammatory cells is not a recognized specific therapeutic target, such as a receptor, enzyme, or individual protein, in biomedical literature; instead, it appears to be a misnomer or overly broad term likely intended to refer to immune cells like macrophages, T helper cells (Th1, Th17), and dendritic cells that produce and release pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF-α). These cells orchestrate innate and adaptive immune responses by secreting signaling molecules that promote inflammation in response to infection, injury, or pathogens, recruiting additional immune cells, inducing fever, and facilitating pathogen clearance or tissue repair. In disease contexts, overactivation of these cells drives chronic inflammation in conditions like autoimmune diseases, sepsis, and cytokine storms seen in viral infections (e.g., SARS-CoV-2), where excessive cytokine release leads to tissue damage and poor prognosis. While individual cytokines or their receptors (e.g., TNF-α receptor, IL-6 receptor) are established therapeutic targets for drugs like monoclonal antibodies (e.g., adalimumab for TNF-α), no drugs directly target "pro-inflammatory cells" as a class; modulation typically occurs indirectly via cytokine blockade. This lack of specificity makes "pro-inflammatory cells" unsuitable as a canonical target, with research focusing on cell subsets or molecular mediators instead. Correcting to specific cytokines or cell types (e.g., M1 macrophages) would enable targeted drug development.
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