Impaired innate immunity in Crohn's disease.
The aetiology of Crohn's disease--a chronic intestinal disorder that involves an immune response against the commensal bacterial flora--remains fiercely debated. Two hypotheses exist: (i) those who think that the disease is caused by genetic defects that produce exaggerated innate responses to the flora, leading to excessive inflammation; and (ii) those who think that the genetic defects cause diminished inflammatory responses, in turn leading to uncontrolled accumulation of the inducer stimuli and, thus, activation of the adaptive immune system. Importantly, Marks and colleagues have recently investigated the immune response of Crohn's disease patients directly, convincingly showing impaired innate immunity.
Comalada
Mònica
M
Department of Pharmacology, School of Pharmacy, University of Granada, Campus Universitario La Cartuja s/n, Granada 18071, Spain.
Peppelenbosch
Maikel P
MP
D000119:Acetylmuramyl-Alanyl-Isoglutamine / Q000276:immunology; D000818:Animals; D001419:Bacteria / Q000276:immunology; D003424:Crohn Disease / Q000235:genetics* / Q000276:immunology* / Q000628:therapy; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology*; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000276:immunology / Q000502:physiology; D051379:Mice; D008954:Models, Biological; D016328:NF-kappa B / Q000378:metabolism; D053473:Nod2 Signaling Adaptor Protein; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D051195:Toll-Like Receptor 2 / Q000502:physiology; D051197:Toll-Like Receptor 4 / Q000502:physiology
D047908:Intracellular Signaling Peptides and Proteins; D016328:NF-kappa B; C429018:NOD2 protein, human; D053473:Nod2 Signaling Adaptor Protein; C495945:Nod2 protein, mouse; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D000119:Acetylmuramyl-Alanyl-Isoglutamine