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The term 'Immune system via cell-cell interfaces and soluble mediators' refers to the comprehensive physiological network governing immune responses through direct physical contact between cells and the secretion of signaling molecules. This system encompasses the immunological synapse—where cells like T cells and antigen-presenting cells exchange signals—and the action of soluble mediators such as cytokines, chemokines, and interferons (Janeway's Immunobiology, 9th Ed). It is not a single therapeutic target but a high-level biological classification that includes thousands of distinct molecular entities, including receptors (e.g., PD-1, TNF receptors) and ligands (e.g., IL-6, IFN-gamma). Dysregulation of these interfaces and mediators is central to the pathogenesis of autoimmune disorders, chronic inflammatory diseases, and the evasion of immune surveillance by tumors (Nature Reviews Immunology, 2018). While numerous pharmacological agents target specific components within this system to achieve therapeutic effects, the system itself represents a broad biological pathway rather than a discrete, druggable molecule. Consequently, in drug discovery and clinical databases, this phrase is typically used as a category for mechanisms of action or therapeutic areas rather than a specific protein target.
Modulation of immune cell interactions and signaling through the agonism or antagonism of specific receptors, ligands, and intracellular signaling proteins within the immune network.
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