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1 B/c mice but did not cause necrosis in their ilea.
2 g that the cells that induce necrosis in the ilea after infection are CD4+ alpha/beta T cells.
3 nst death and development of necrosis in the ilea after infection, studies were performed using athym
4  in the pathology scores was observed in the ilea and ceca of mice infected with the ibeA mutant.
5 ed significantly less Nod2 in their terminal ilea, and complementation of commensal bacteria into ger
6 r of split 1:mouse atonal homolog 1 ratio in ilea from Msi1-overexpressing mice implicated Notch sign
7                                              Ilea from native SAMP mice and SAMP recipients of wild-t
8  cell subset(s) that induces necrosis of the ilea in B6 mice, we examined histological changes of the
9  time to death and prevented necrosis in the ilea in these mice.
10 A levels were significantly increased in the ilea of 80% of germ-free SAMP1/Fc mice examined compared
11 cate that IFN-gamma mediates necrosis in the ilea of B6 mice after infection.
12 ithelial adherens and tight junctions in the ilea of coinfected mice.
13                                           In ilea of Crohn's disease patients, increased expression o
14 ly correlated with secretory cell markers in ilea of healthy individuals and Crohn's disease patients
15 5214 and GDS2642 of RNA expression data from ilea of healthy individuals undergoing screening colonos
16 IL1 receptor; macrophages were depleted from ilea of mice using clodronate-containing liposomes.
17 involved in T cell receptor signaling in the ilea of mice with aGVHD.
18 bers of CD103+ DCs decreased in the inflamed ilea of mice with chronic disease; RA synthetic machiner
19                                              Ilea of mutant mice displayed increased expression of en
20 sis of intestinal bacteria from the terminal ilea of Nod2-deficient mice showed that they harbor an i
21 ro, intestinal crypts isolated from terminal ilea of Nod2-deficient mice were unable to kill bacteria
22 CD ilea that are preserved in the unaffected ilea of patients with colon-only CD but not present in t
23 he bacterial concentration in the jejuna and ilea of pigs expressing IMTGP was significantly greater
24 d within draining mesenteric lymph nodes and ilea of SAMP versus AKR (parental control) mice early, d
25           RELMbeta was highly induced in the ilea of SAMP1/Fc mice beginning at age 5 wk, coincident
26 ytokines IL-6, IL-1beta and TNF-alpha in the ilea of Tat+ mice and by enteric glia.
27  These results indicate that necrosis in the ilea of the B6 mice was not due to destruction of tissue
28  numbers of tachyzoites were observed in the ilea of the former than the latter mice.
29 dministration recapitulated these effects in ilea of uninflamed (parental) control AKR/J mice.
30              Histological examination of the ilea of younger animals revealed no differences in the n
31 and microbial communities in the affected CD ilea that are preserved in the unaffected ilea of patien
32 ontaining pETR14 was recoverable from rabbit ilea up to 5 days after oral inoculation.
33                              Necrosis in the ilea was observed in control B6 but not in athymic B6 mi
34                                     Terminal ilea were collected for histologic assessment of inflamm
35 NMDA stimulation induces opioid release, (1) ilea were exposed to NMDA (100 micromol/L) and D-serine
36                                     Terminal ilea were harvested for histological scoring, and lamina
37 crosis of the villi and mucosal cells in the ilea were observed in B6 but not in BALB/c mice.
38 CD4+ T cells did not develop necrosis in the ilea, whereas wild-type control mice and mice deficient