The Profile of Chemokine Expression in Rat-To-Mouse Skin Xenograft.
- Author:
Eun Mi LEE
1
;
Jae Young KIM
;
Curie AHN
;
Donghee KIM
;
Minae SONG
;
Jaeseok YANG
;
Jongwon HA
;
Sang Joon KIM
;
Byung Hee OH
;
Jung Sang LEE
Author Information
1. Transplantation Research Institute, Seoul National University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Chemokines;
Skin;
Xenotransplantation
- MeSH:
Allografts;
Chemokine CCL5;
Chemokines;
Heterografts*;
Leukocytes;
Neutrophils;
RNA, Messenger;
Skin*;
T-Lymphocytes;
Transplantation, Heterologous
- From:The Journal of the Korean Society for Transplantation
2003;17(1):7-14
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The host immune responses to skin xenografts are known to be much stronger than those to allografts. The possible reasons for that, however, are unclear. We hypothesized that chemokines trafficking leukocytes may be involved in stronger xenograft rejection process as compared to allograft rejection. METHODS: Thus, we evaluated the profiles of chemokine expression and cellular infiltration in the skin xenografts and compared to those in fully allogeneic skingrafts. RESULTS: At day 5, post-transplantation the heavier cellular infiltration of CD4+, CD8+ T cells and neutrophils into xenografts was found as compared to allografts. Similarly, more CD8+ T, CD11b+ and MOMA-2+ cells were found to infiltrate into xenografts than allografts at day 7. The xenograft showed earlier and stronger mRNA expression of chemokines such as MCP-1, IP-10 and MIG. In the late phase of xenograft rejection, strong expression of RANTES and MIP-1a was noted. In xenografts, the time of expression of IP-10 and MIG was correlated with the time of infiltration of CD4+, CD8+ cells and neutrophils whereas, the expression patterns of RANTES and MIP-1a were similar to the infiltration patterns of CD11b+ and MOMA-2+ cells. CONCLUSION: These results suggest that the prompt xenograft cellular rejection as compared to the allograft rejection may be related to the rapid induction of pro-inflammatory chemokines such as MCP-1, IP-10 and MIG in the early phase and resultant significant infiltration of CD4+ and CD8+ T cells and neutrophils.
