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Organ-Specific Differences in the Function of MCP-1 and CXCR3 During Cardiac and Skin Allograft Rejection

Background. Chemokines are well-established to function in the recruitment of leukocytes into allografts in the course of rejection. Moreover, some studies have indicated that there are organ-specific differences in chemokine function, but the mechanism accounting for this difference is not known. Methods. Fully major histocompatibility complex–mismatched vascularized cardiac transplants or skin transplants were performed using BALB/c (H-2d), C57BL/6 (H-2b), MCP-1−/− (H-2b) and CXCR3−/− (H-2b) mice as donors or recipients. Also, skin grafts (H-2b) were placed onto SCID mice (H-2d) that received BALB/c splenocytes (H-2d) by adoptive transfer either at the time of transplantation, or after a period of 28 days. Results. Cardiac allografts in MCP-1−/− recipients survived significantly longer (P<0.0005) than wild-type (WT) controls. However, there was no prolongation of survival when MCP-1−/− grafts were used a donors in WT mice. In contrast, the absence of donor but not recipient MCP-1 prolonged skin allograft survival. WT donor cardiac grafts in CXCR3−/− recipients had a modest prolongation of survival (P<0.0005), whereas CXCR3−/− donor cardiac grafts in WT recipients were rejected similar to controls. Also, while recipient CXCR3 had no effect on the rejection of skin, CXCR3−/− donor skin grafts survived significantly longer than WT controls. This survival advantage was lost when vascularized CXCR3−/− skin grafts were used as donors in the SCID model of rejection. Conclusion. Recipient derived MCP-1 and CXCR3 are functional in the rejection of vascularized, but not nonvascularized, allografts. In contrast, donor-derived MCP-1 and CXCR3 are functional in nonvascularized, but not vascularized grafts.