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The gut microbiota comprises trillions of symbiotic microorganisms that reside in the gastrointestinal tract and interact dynamically with both commensal and pathogenic bacteria as well as with the host’s immune system cells. These interactions are essential for maintaining intestinal homeostasis, regulating local and systemic immune responses, and protecting against infection and inflammation[1][2][3][4][5][6]. Disruptions to this balance—such as an overrepresentation of pathogenic bacteria or a loss of normal gut microbial diversity (dysbiosis)—can impair epithelial barrier function, exacerbate inflammation, and contribute to diseases including autoimmune disorders, infections, metabolic syndromes (like type 2 diabetes), cardiovascular disease, and cancer[1][3][4]. Immune system cells—spanning innate (macrophages, dendritic cells, innate lymphoid cells) and adaptive (T and B lymphocytes, especially IgA plasma cells)—continuously interact with gut microbiota and their metabolites to regulate homeostasis, tolerance, and defense against pathogens[2][3][4]. Secretory immunoglobulin A (IgA) plays a central role in mucosal immunity, both by neutralizing pathogens and by shaping the commensal microbial community[1][3][5]. While this biological network is a critical area of research and therapeutic interest, it does not correspond to a single molecule, gene, or classical druggable target. Consequently, standard pharmacological targeting, as applied to receptors or single enzymes, is not appropriate for this broad “target.”
Modulation of immune cell signaling by microbial metabolites; Dysbiosis-targeting therapies (e.g., fecal microbiota transplantation, prebiotics, probiotics); Antibiotic effects on pathogen balance
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