IL-4 expression delays eosinophil-independent vasculopathy and fibrosis during allograft rejection in the mouse.
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.
Roberts
Edda M
EM
Department of Immunology, IMM-23, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA.
Hall
De Shon
DS
Ferguson
Sharon
S
Minson
Susan
S
Davies
Joanna D
JD
D000818:Animals; D002985:Clinical Protocols / Q000592:standards; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004804:Eosinophils / Q000502:physiology; D005355:Fibrosis / Q000209:etiology*; D006084:Graft Rejection / Q000209:etiology*; D015847:Interleukin-4 / Q000502:physiology*; D016030:Kidney Transplantation / Q000009:adverse effects; D051379:Mice; D008815:Mice, Inbred Strains; D008954:Models, Biological; D013154:Spleen / Q000166:cytology / Q000378:metabolism / Q000637:transplantation; D014184:Transplantation, Homologous / Q000009:adverse effects; D014652:Vascular Diseases / Q000209:etiology*
D016207:Cytokines; D015847:Interleukin-4