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The gut microbiome-host immune axis is a complex, bidirectional communication network between the gastrointestinal microbiota and the host's innate and adaptive immune systems. This ecosystem is critical for the maturation of lymphoid tissues and the induction of immune tolerance, primarily through the production of metabolites like short-chain fatty acids (SCFAs) that promote regulatory T cell (Treg) differentiation [1][2]. Disruptions in this balance, known as dysbiosis, are implicated in the pathogenesis of numerous diseases, including inflammatory bowel disease (IBD), allergies, and autoimmune disorders [3][4]. Pharmacological modulation of this axis is an emerging field, utilizing live biotherapeutic products (LBPs), fecal microbiota transplantation (FMT), and prebiotics to restore homeostatic immune signaling [5]. Unlike traditional single-molecule targets, this axis represents a systemic interface involving diverse microbial species and host signaling pathways [6].
Modulation of regulatory T cells (Tregs) via short-chain fatty acids (SCFAs), activation of pattern recognition receptors (PRRs) such as TLRs and NLRs, and competitive exclusion of pathogenic microorganisms.
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