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Proinflammatory factors are a heterogeneous group of signaling molecules, including cytokines, chemokines, and lipid mediators, that initiate and propagate inflammatory responses in the body. They are primarily secreted by activated immune cells, such as macrophages, neutrophils, and lymphocytes, in response to pathogens, tissue damage, or cellular stress [1, 7]. Key members of this class, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6), bind to specific cell-surface receptors to activate downstream signaling cascades, most notably the NF-κB and JAK-STAT pathways [13, 14]. While these factors are essential for mounting an effective immune response and promoting tissue repair, their chronic or excessive production is a central driver of many inflammatory and autoimmune diseases, including rheumatoid arthritis, inflammatory bowel disease, and atherosclerosis [2, 3]. Consequently, these molecules and their receptors are major therapeutic targets; biological drugs like monoclonal antibodies and small-molecule inhibitors are widely used to neutralize their activity [2, 5]. However, systemic inhibition of these factors can lead to significant clinical challenges, including increased susceptibility to opportunistic infections and impaired host defense mechanisms [1, 15].
Neutralization of circulating proinflammatory signaling molecules or competitive blockade of their respective cell-surface receptors to inhibit downstream inflammatory signal transduction.
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