Mucosal immune response in biology, disease prevention and treatment Original paper

What was reviewed?

This paper reviewed the biological mechanisms that govern mucosal immune responses and their role in disease prevention, immune regulation, and therapeutic development, with a central focus on interactions between the host immune system and resident microbiota at mucosal surfaces. The authors synthesized immunology, microbiology, and translational research to explain how mucosal tissues such as the gastrointestinal, respiratory, and urogenital tracts function as highly specialized immune environments. The review emphasized that mucosal immunity must maintain a constant balance between immune tolerance toward commensal microorganisms and food antigens, and rapid, effective defense against pathogens. Rather than portraying the microbiome as a secondary modifier, the article positioned commensal microbes as essential architects of mucosal immune development, shaping epithelial integrity, immune cell differentiation, and immune signaling pathways throughout life.

Who was reviewed?

The review drew upon studies involving healthy human populations, patients with mucosal inflammatory and infectious diseases, and experimental animal models used to dissect immune–microbial interactions. Evidence was synthesized from neonatal, pediatric, and adult cohorts to illustrate how early-life microbial exposure influences long-term immune programming at mucosal sites. The authors also integrated findings from individuals with inflammatory bowel disease, respiratory tract infections, food allergies, and autoimmune conditions, highlighting how altered mucosal immunity and disrupted microbiome composition contribute to disease susceptibility, persistence, and severity.

What were the most important findings?

The review demonstrated that functional mucosal immunity depends on continuous bidirectional communication between commensal microorganisms and host immune cells. Commensal bacteria actively promote the maturation of gut-associated lymphoid tissue, stimulate IgA production, and regulate the balance between regulatory T cells and pro-inflammatory effector T cells. Major microbial associations included short-chain fatty acid–producing bacteria, which enhance epithelial barrier integrity and drive regulatory immune pathways, and segmented filamentous bacteria, which induce Th17 cell differentiation critical for mucosal defense. Microbial metabolites emerged as key immune modulators, influencing cytokine signaling, antigen presentation, and immune tolerance. When these microbial signals are disrupted by antibiotics, dietary changes, or infection, the mucosal barrier becomes compromised, inflammatory responses intensify, and susceptibility to pathogens increases. The review also emphasized that mucosal immune responses are anatomically compartmentalized, meaning that immune regulation in one mucosal site can have downstream systemic effects.

What are the greatest implications of this review?

The most significant implication for clinical practice is that effective immune protection and disease management at mucosal surfaces require preservation of microbial diversity and function. The findings explain why mucosal vaccines often induce stronger and more durable immune responses and why treatments that ignore the microbiome may fail or worsen inflammation. This review supports microbiome-informed clinical strategies, including mucosal vaccine design, probiotic and postbiotic therapies, and immune tolerance–inducing interventions. For clinicians, the paper reinforces that mucosal immune resilience depends on maintaining a stable and functional host–microbiome relationship rather than targeting immune pathways in isolation.