
Abstract: The immense microbiological load of the gastrointestinal tract poses a daunting challenge for the mucosal immune system: whereas it should tolerate the vast number of commensal bacteria, it should adequately attack pathogenic organisms. Millions of years of co‐evolution have produced an intricate system in which interactions between the endogenous flora and mucosal immune system manage to perform this difficult balancing act. When components of this interaction are defective, for instance by mutation, inflammatory bowel disease may result. In the present review, we comprehensively discuss the mucosal immune system in the context of Crohn's disease (CD) and its genetic risk factors, describe the clinical management of the disease, and discuss how knowledge of the mucosal immune system may yield novel therapeutical avenues for dealing with this debilitating disease.
HELPER TYPE-1 RESPONSES, NF-KAPPA-B, Nod2 Signaling Adaptor Protein, pattern recognition and host bacterial cells, DENDRITIC CELLS, Crohn Disease, mucosal immunology, LYMPHOID-TISSUE GALT, ESCHERICHIA-COLI STRAINS, Humans, dendritic cells, REGULATORY T-CELLS, TOLL-LIKE RECEPTORS, Inflammation, CUTTING EDGE, Toll-Like Receptors, Intracellular Signaling Peptides and Proteins, Bacterial Infections, Immunity, Innate, Crohn's disease, INTESTINAL EPITHELIAL-CELLS, INFLAMMATORY-BOWEL-DISEASE
HELPER TYPE-1 RESPONSES, NF-KAPPA-B, Nod2 Signaling Adaptor Protein, pattern recognition and host bacterial cells, DENDRITIC CELLS, Crohn Disease, mucosal immunology, LYMPHOID-TISSUE GALT, ESCHERICHIA-COLI STRAINS, Humans, dendritic cells, REGULATORY T-CELLS, TOLL-LIKE RECEPTORS, Inflammation, CUTTING EDGE, Toll-Like Receptors, Intracellular Signaling Peptides and Proteins, Bacterial Infections, Immunity, Innate, Crohn's disease, INTESTINAL EPITHELIAL-CELLS, INFLAMMATORY-BOWEL-DISEASE
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