CD44 EXPRESSION IN REJECTING RAT SMALL-BOWEL ALLOGRAFTS

Citation
Cr. Uff et al., CD44 EXPRESSION IN REJECTING RAT SMALL-BOWEL ALLOGRAFTS, Transplantation, 60(9), 1995, pp. 985-989
Citations number
29
Categorie Soggetti
Immunology,Surgery,Transplantation
Journal title
ISSN journal
00411337
Volume
60
Issue
9
Year of publication
1995
Pages
985 - 989
Database
ISI
SICI code
0041-1337(1995)60:9<985:CEIRRS>2.0.ZU;2-P
Abstract
CD44 is a widely expressed cell surface protein that recognizes multip le ligands and is involved in extra- and intercellular adhesion. The p recise role of CD44 in immune interactions is currently unknown, but i t is believed to be a homing receptor involved in lymphocyte trafficki ng and inflammatory responses. This study investigated CD44 expression in intestinal tissue after heterotopic rat small bowel transplantatio n and assessed the effect of transplantation on intestinal epithelial cell proliferation using an antibody to the nuclear activation Ag Ki67 . Lamina propria and intestinal epithelial cell expression of CD44 was graded blindly by five observers, and villus epithelial cells were no ted as being positive or negative for Ki67 staining. CD44 expression w as high in the lamina propria of both allografted and isografted anima ls; however, there was no significant difference between the two group s, in contrast, the expression of CD44 on the villus epithelium was gr eater in allografted animals and progressed toward the villus tips as rejection developed, declining thereafter because of loss of villus in tegrity, Ki67 positivity was also greater in allografted animals but d id not progress toward the villus tip. This is the first reported obse rvation of CD44 expression on intestinal epithelium that is not restri cted to the crypts, The findings indicate the involvement of CD44 in t he rejection process and demonstrate changes in the proliferative prof ile of rejecting small intestinal epithelium, Further studies into adh esion molecules, such as CD44, may help to improve understanding of gr aft failure and promote the development of new therapeutic approaches for controlling and preventing graft rejection.