Journal of Clinical Immunology

, Volume 23, Issue 2, pp 119–131

IL-4 Expression Delays Eosinophil-Independent Vasculopathy and Fibrosis During Allograft Rejection in the Mouse

Authors

  • Edda M. Roberts
    • Department of Immunology, IMM-23The Scripps Research Institute
  • De Shon Hall
    • Department of Immunology, IMM-23The Scripps Research Institute
  • Sharon Ferguson
    • Department of Immunology, IMM-23The Scripps Research Institute
  • Susan Minson
    • Department of Immunology, IMM-23The Scripps Research Institute
    • Department of Immunology, IMM-23The Scripps Research Institute
Article

DOI: 10.1023/A:1022576828317

Cite this article as:
Roberts, E.M., Hall, D.S., Ferguson, S. et al. J Clin Immunol (2003) 23: 119. doi:10.1023/A:1022576828317

Abstract

Transplant vasculopathy in the mouse is thought to be dependent on IL-4 and mediated by IL-5 and eosinophils, whereas in the rat and human systems, IL-4 is associated with the absence of transplant vasculopathy and down-regulation of a Th1-type response. In this study we tested the possibility that the apparent difference in the role of IL-4 in transplant vasculopathy is related to protocol differences rather than to the species being studied. Using a protocol that closely resembles that used in rat and human studies, we developed a model of transplant vasculopathy in the mouse that is associated with Th1-type cytokines and independent of IL-5 and eosinophil infiltration. In this model IL-4 promotes a significant delay in vasculopathy in the graft (P = 0.04) and a decrease in the incidence of allograft rejection (P = 0.02). The data suggest that the role of IL-4 in transplant vasculopathy can be controlled by the protocol used to treat the transplant recipient.

TransplantationvasculopathyMHCTh1/Th2 cellscytokines

Copyright information

© Plenum Publishing Corporation 2003