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
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.