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C. A. Medina-Mendez, A. Sidani, G. Amescua, V. L. Perez; Role of CXCL10/IP10 Production in High Risk Corneal Allograft Transplantation. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3721.
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We have previously reported that CXCL10/IP10 is up regulated in high risk corneal allografts after transplantation. The goal of this work is to understand how its production regulates graft rejection.
Fully MHC mismatched corneal allografts (Balb/c to C57BL6) were performed in vascularized high risk recipients treated with systemic or local anti-CXCL10 antibody or control. CXCL10/IP10 KO mice were also used as high risk recipients. Graft survival was monitored and quantification of infiltrating inflammatory cells was performed by immunohistochemistry. To directly test the role of CXCL10, high risk recipients were also treated locally with recombinant CXCL10/IP10.
High risk corneal allograft recipients in which CXCL10/IP10 was systemically and locally neutralized with anti-IP10 antibody had an increased rate of rejection. Similar results were observed in CXCL10/IP10 KO recipients. Graft rejection correlated with an increased recruitment of macrophages and T cells into the corneal allograft. In contrast, when high risk corneal allograft recipients were treated with recombinant CXCL10/IP10, graft survival was prolonged.
Our data suggests that the production of CXCL10/IP10 may alter the recruitment of regulatory and effector cells into the graft resulting in graft protection.
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