Innate immunity in Crohn's disease: the reverse side of the medal.
The etiology of Crohn's disease (CD) remains poorly understood. Both mice and human studies suspected a perverse link between the microbiota and the lining of the gut mucosa. There is now emerging evidence that suggests that such a pathologic condition might result from an overly aggressive immune response to microbial antigens in genetically predisposed individuals. However, the multiple pathophysiologic processing steps linking environmental exposure to the clinical expression of CD are, for the most part, unknown. Herein, we review evidences reflecting a general causing defect of the innate immune function of the intestinal mucosa of CD patients, which might lead to a sustained microbial-induced inflammatory response. Changing the paradigms of CD pathophysiology might lead to entirely new therapeutic approaches aiming to boost the innate immune response.
Dessein
Rodrigue
R
INSERM, U801, Université Lille 2, Lille, France.
Chamaillard
Mathias
M
Danese
Silvio
S
D000818:Animals; D003424:Crohn Disease / Q000235:genetics / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology*; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics / Q000276:immunology; D007413:Intestinal Mucosa / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D051379:Mice; D053473:Nod2 Signaling Adaptor Protein / Q000235:genetics / Q000276:immunology; D010539:Permeability
D053473:Nod2 Signaling Adaptor Protein