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J Am Soc Nephrol 15:1853-1861, 2004
© 2004 American Society of Nephrology

BASIC SCIENCE

Differential Expression of Chemokines and Chemokine Receptors in Murine Islet Allografts: The Role of CCR2 and CCR5 Signaling Pathways

Bernd Schröppel*, Nan Zhang{dagger}, Peng Chen*, Weiping Zang*, Dongmei Chen{dagger}, Kelly L. Hudkins{ddagger}, William A. Kuziel§, Randall Sung{dagger}, Jonathan S. Bromberg{dagger} and Barbara Murphy*,¶

*Division of Nephrology, Mount Sinai School of Medicine, New York, {dagger}Carl C. Icahn Center for Gene Therapy and Molecular Medicine, Recanati/Miller Transplantation Institute Mount Sinai School of Medicine, New York, New York; {ddagger}Department of Pathology, University of Washington, Seattle, Washington; and §Department of Microbiology, Institute for Cellular and Molecular Biology, University of Texas, Austin, Texas.

Correspondence to Dr. Barbara Murphy, Division of Nephrology, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1243, New York, NY 10029-6574. Phone: 212-241-5850; Fax: 212-987-0389; E-mail: barbara.murphy{at}mssm.edu

ABSTRACT. Chemokines and their receptors play a pivotal role in the initiation and amplification of the immune response. Investigated was their differential expression after syngeneic and allogeneic islet transplantation. During the 7 d after transplantation, the chemokines MCP-1, MCP-2, RANTES, MIG, IP-10, I-TAC, and two CC chemokine receptors CCR2 and CCR5 were highly expressed in allografts when compared with isografts. Disrupting the CCR2 and CCR5 pathways individually resulted in prolongation of the survival time 16.1 ± 0.4 and 15.8 ± 0.9 d, respectively, of fully major histocompatibility complex–mismatched islet grafts compared with wild-type controls (11.2 ± 1.0 d). Blockade of both receptors had no synergistic effect. Rapamycin-treated wild-type recipients rejected their grafts at 17.4 ± 2.2 d, in contrast to rapamycin-treated CCR2–/– recipients at 38 ± 8.6 d (P = 0.025). The disruption of the CCR2 and CCR5 signaling, alone or in combination, moderately prolong islet allograft survival. However, the combination of low-dose immunosuppression and targeting of CCR2 greatly augmented islet graft survival.




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