To identify the molecular mechanism which primarily plays a role in the pat
hogenesis of Crohn's disease (CD) without prior hypothesis, differential di
splay method was employed to detect differentially expressed genes between
the inflamed and uninflamed colonic samples from one patient with CD. The m
RNA levels of these genes were subsequently semi-quantitated in affected an
d unaffected tissues from six patients using reverse transcriptase polymera
se chain reaction (RT-PCR). Six genes including long form FLICE inhibitory
protein (FLIPL) were found to be consistently overexpressed in the inflamed
colonic CD tissues. Immunohistochemical studies revealed that FLIPL expres
sing cells were lamina propria lymphocytes (LPLs). The present study sugges
ted that overexpression of FLIPL in the LPLs may be involved in the pathoge
nesis of CD through defective activation-induced cell death. In addition, t
his study provided evidence for a possible role of several previously unsus
pected genes in the pathogenesis of CD. (C) 2001 Academic Press.