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152 153 Intestinal Disease Meeting Berlin 2006 - Dr. Falk Pharma ...

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Session 1<br />

Congress Short Report <strong>Falk</strong> Symposium <strong>153</strong><br />

<strong>Falk</strong> Symposium <strong>153</strong><br />

Immunoregulation in Inflammatory Bowel <strong>Disease</strong>s –<br />

Current Understanding and Innovation<br />

<strong>Berlin</strong>, May 6–7, <strong>2006</strong><br />

Advances in the Pathogenesis<br />

of IBD<br />

Chair:<br />

A. Dignass, Frankfurt<br />

D. Rachmilewitz, Jerusalem<br />

Inflammatory bowel diseases:<br />

strong genetic components<br />

Inflammatory bowel diseases (IBD) such as<br />

Crohn’s disease (CD) and ulcerative colitis (UC)<br />

usually manifest themselves in adolescents or<br />

young adults. Their incidence has been increasing<br />

over the past decades and, according to<br />

S. Schreiber (Kiel), it occurs more frequently in<br />

some families. This, together with the high concordance<br />

in monozygotic twins (over 55%),<br />

which is not observed in fraternal twins (under<br />

5%), supports the hypothesized strong genetic<br />

component of these diseases.<br />

IBD are polygenetic diseases, although recent research<br />

has identified the NOD2 (CARD15) gene<br />

that potentially acts as a trigger in the pathogenesis<br />

of Crohn’s disease (figure 18). According to<br />

S. Schreiber, NOD2 belongs to a large family of<br />

S. Schreiber<br />

proteins involved in defending the organism from<br />

bacterial invasion. “NOD2, however, is not by<br />

far the only component of the pathomechanism<br />

of inflammatory bowel diseases,” S. Schreiber<br />

said. Corresponding mutations are involved in<br />

the disease process in less than half of all patients<br />

(figure 19), which means that the search must<br />

continue for further potential pathogenetic<br />

factors.<br />

Like NOD2, some other factors may involve chromosome<br />

16, on which several areas have been<br />

identified that may be involved in the development<br />

of IBD. Here, S. Schreiber said, gene splicing<br />

may play a role. This process, in which RNA<br />

fragments of varying length and corresponding<br />

protein fragments are produced, lends high<br />

plasticity to the human genome.<br />

27

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