SIALYL LEWIS(X)-DEPENDENT AND L-SELECTIN-DEPENDENT SITE-SPECIFIC LYMPHOCYTE EXTRAVASATION INTO RENAL-TRANSPLANTS DURING ACUTE REJECTION

Citation
Jp. Turunen et al., SIALYL LEWIS(X)-DEPENDENT AND L-SELECTIN-DEPENDENT SITE-SPECIFIC LYMPHOCYTE EXTRAVASATION INTO RENAL-TRANSPLANTS DURING ACUTE REJECTION, European Journal of Immunology, 24(5), 1994, pp. 1130-1136
Citations number
55
Categorie Soggetti
Immunology
ISSN journal
00142980
Volume
24
Issue
5
Year of publication
1994
Pages
1130 - 1136
Database
ISI
SICI code
0014-2980(1994)24:5<1130:SLALSL>2.0.ZU;2-C
Abstract
Kidney allograft rejection is an inflammatory process dominated by lym phocytes. During rejection lymphocytes preferentially adhere to the pe ritubular capillary endothelium (PTCE), which acquires morphological f eatures common to high endothelium. These observations indicate that P TCE is the site of lymphocyte entry into the rejecting renal allograft . Of the identified endothelial adhesion molecules, ICAM-1 was already expressed on the endothelium of normal kidneys, and its expression wa s strongly enhanced during rejection without site-specific restriction . VCAM-1 was not expressed on the endothelium of normal or syngeneic k idneys, but its expression was induced during allograft rejection not only in PTCE, but occasionally also on the endothelium of larger vesse ls. Sialyl Lewis(x) (sLe(x)) showed a very restricted pattern of expre ssion; endothelium was sLe(x)-negative both in control and syngeneic k idneys. On the other hand, PTCE reacted strongly with anti-sLe(X) anti body in allografts. When kidney frozen sections were treated with sial idase the binding of lymphocytes decreased by 70%. Low-dose chymotryps in treatment of lymphocytes, known to remove L-selectin from the lymph ocyte surface, decreased their binding to PTCE by 60%. Likewise lympho cyte adhesion to PTCE was inhibited by 70% by anti-sLe(X)- and anti-L- selectin-antibodies and by sLe(X) tetrasaccharide. Finally PTCE in the allografts, but not in syngeneic grafts or normal kidneys, bound an L -selectin-IgG fusion protein, indicating that ligands for L-selectin w ere induced during rejection.