Genetic and pathogenetic insights into inflammatory bowel disease.
Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of the gastrointestinal tract that share clinical and pathologic characteristics. The most credible hypothesis is that CD and UC result from an inappropriate and exaggerated mucosal immune response to normal constituents of the mucosal microflora that is in part genetically determined. However, there is reason to believe that the main pathologic processes in these two diseases are distinct. For example, the CARD15/NOD2 gene has been identified as a susceptibility gene for CD but not for UC. Moreover, the study of patients and mouse models of inflammatory bowel disease has clearly shown that, in CD, the tissue-damaging inflammatory reaction is driven by interleukin-12-activated Th1 cells, whereas a humoral response predominates in UC.
Cattedra di Gastroenterologia, Dipartimento di Medicina Interna, Università Tor Vergata di Roma, Via Monpellier 1, 00133 Rome, Italy. pallone@med.uniroma2.it
Francesco
F
Pallone
Giovanna Del Vecchio
Gdel V
Blanco
Piero
P
Vavassori
Ivan
I
Monteleone
Daniele
D
Fina
Giovanni
G
Monteleone
D000818:Animals; D000917:Antibody Formation; D002352:Carrier Proteins / Q000235:genetics; D003093:Colitis, Ulcerative / Q000235:genetics* / Q000276:immunology*; D003424:Crohn Disease / Q000235:genetics* / Q000276:immunology*; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D053473:Nod2 Signaling Adaptor Protein; D018417:Th1 Cells / Q000276:immunology
D002352:Carrier Proteins; D047908:Intracellular Signaling Peptides and Proteins; C429018:NOD2 protein, human; D053473:Nod2 Signaling Adaptor Protein