Modulation of the immune response by fetal kidney allografts.
Fetal kidneys modulate the allogeneic immune response by a synergistic effect: first, fetal kidney tissue tropism is abrogated by the initial relative lack of adhesion molecules. Second, the reduced expression of major histocompatibility complex (MHC) determinants is less effective in inducing the alloantigen-primed T cell response, which in turn induces the downregulation of Th1 cytokines, beta chemokines, and Fas ligand, but spares protective Th2 cytokines, and leads to minimal induction of MHC and adhesion molecules on immature renal parenchymal elements. Thus, at the onset and during this altered rejection process, cellular recruitment to the fetal renal site is less prominent than to the adult renal tissue, and effector cells in the fetal graft are less activated.
Dekel
B
B
Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel.
Passwell
J H
JH
Reisner
Y
Y
D000328:Adult; D000818:Animals; D015815:Cell Adhesion Molecules / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D016332:Fetal Tissue Transplantation / Q000276:immunology*; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D007668:Kidney / Q000196:embryology* / Q000276:immunology / Q000473:pathology; D016030:Kidney Transplantation / Q000276:immunology*; D007962:Leukocytes / Q000276:immunology; D051379:Mice; D051381:Rats; D017207:Rats, Sprague-Dawley
D015815:Cell Adhesion Molecules; D016207:Cytokines; D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II