Modulation of the immune response by fetal kidney allografts

Fetal kidneys modulate the allogeneic immune response by a synergistic effe ct: first, fetal kidney tissue tropism is abrogated by the initial relative lack of adhesion molecules. Second, the reduced expression of major histoc ompatibility complex (MHC) determinants is less effective in inducing the a lloantigen-primed T cell response, which in turn induces the downregulation of Th 1 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 f etal graft are less activated.