Changes of CD8+CD28- T regulatory cells in rat model of colitis induced by 2,4-dinitrofluorobenzene.

Abstract:

AIM:To determine the changes of CD8+ T subsets especially CD8+CD28- T regulatory cells in rat model of experimental colitis induced by 2,4-dinitrofluorobenzene (DNFB). METHODS:The rat model of experimental colitis was induced by enema with DNFB. Ten days later, colonic intraepithelial and splenic lymphocytes were isolated from colitis animals (n=16) and controls (n=8). The proportion of CD8+ T cells, CD8+CD28+ T cells and CD8+CD28- T regulatory cells were determined by flow cytometry. RESULTS:The model of experimental colitis was successfully established by DNFB that was demonstrated by bloody diarrhea, weight loss and colonic histopathology. The proportion of CD8+ T cells in either splenic or colonic intraepithelial lymphocytes was not significantly different between colitis animals and controls (spleen: 34.6+/-7.24% vs 33.5+/-9.41%, colon: 14.0+/-8.93% vs 18.0+/-4.06%, P>0.05). But CD8+CD28- T regulatory cells from colitis animals were significantly more than those from controls (spleen: 11.3+/-2.26% vs 5.64+/-1.01%, colon: 6.50+/-5.37% vs 1.07+/-0.65%, P<0.05). In contrast, CD8+CD28+ T cells from colitis animals were less than those from controls (spleen: 23.3+/-6.14% vs 27.8+/-9.70%, P=0.06; colon: 7.52+/-4.18% vs 16.9+/-4.07%, P<0.05). The proportion of CD8+CD28- T regulatory cells in splenic and colon intraepithelial CD8+ T cells from colitis animals was higher than that from controls (spleen: 33.3+/-5.49% vs 18.4+/-7.26%, colon: 46.0+/-14.3% vs 6.10+/-3.72%, P<0.005). CONCLUSION:Experimental colitis of rats can be induced by DNFB with simplicity and good reproducibility. The proportion of CD8+CD28- T regulatory cells in rats with experimental colitis is increased, which may be associated with the pathogenesis of colitis.

journal_name

World J Gastroenterol

authors

Xiao WB,Liu YL

doi

10.3748/wjg.v9.i11.2528

keywords:

subject

Has Abstract

pub_date

2003-11-01 00:00:00

pages

2528-32

issue

11

eissn

1007-9327

issn

2219-2840

journal_volume

9

pub_type

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