title: Prope tolerance with induction using Campath 1H and low-dose cyclosporin monotherapy in 31 cadaveric renal allograft recipients.
abstract: The last 40 years has been a period of remarkable evolution of organ transplantation from nothing to a well-established form of treatment with good short-term and tolerable long-term results. Nevertheless by ten years approximately 50% of grafts will have been lost due, mainly, to chronic rejection or the side-effects of immunosuppressive therapy. We now have a number of extremely powerful immunosuppressive drugs and antibodies with different mechanisms of action and the stage is set for a move from current continuous high dose immunosuppressive maintenance therapy to low dose or no maintenance immunosuppression. True tolerance can occur in man, examples being successful bone marrow transplantation and patients with liver grafts who have stopped immunosuppression after years of good function. The antibody Campath 1H with a unique target CH52 on T & B lymphocytes and monocytes has been used to eliminate lymphocytes from the blood for a month in patients with renal allografts who have then been maintained on half dose Cyclosporin without any other maintenance drug. The results with a mean two year follow-up have been encouraging, 29 patients having good function without receiving maintenance steroids. It is likely that this protocol could be improved since dosage timing and various minimal maintenance immunosuppressive protocols have not been fully investigated. This almost or "Prope" tolerance could be a major step forward providing a better quality of life for patients and inexpensive maintenance immunosuppression.
authors.affiliation: Department of Surgery, Addenbrooke's Hospital, UK.
authors.forename: R
authors.initials: R
authors.lastname: Calne
authors.forename: S D
authors.initials: SD
authors.lastname: Moffatt
authors.forename: P J
authors.initials: PJ
authors.lastname: Friend
authors.forename: N V
authors.initials: NV
authors.lastname: Jamieson
authors.forename: J A
authors.initials: JA
authors.lastname: Bradley
authors.forename: G
authors.initials: G
authors.lastname: Hale
authors.forename: J
authors.initials: J
authors.lastname: Firth
authors.forename: J
authors.initials: J
authors.lastname: Bradley
authors.forename: K G
authors.initials: KG
authors.lastname: Smith
authors.forename: H
authors.initials: H
authors.lastname: Waldmann
mesh_terms: D000328:Adult; D000368:Aged; D000074323:Alemtuzumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm / Q000627:therapeutic use*; D015703:Antigens, CD / Q000276:immunology; D000951:Antigens, Neoplasm; D000074301:CD52 Antigen; D002102:Cadaver; D016572:Cyclosporine / Q000008:administration & dosage*; D005260:Female; D006023:Glycoproteins / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance; D007166:Immunosuppressive Agents / Q000008:administration & dosage*; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D014184:Transplantation, Homologous
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm; D015703:Antigens, CD; D000951:Antigens, Neoplasm; D000074301:CD52 Antigen; C000613862:CD52 protein, human; D006023:Glycoproteins; D007166:Immunosuppressive Agents; D000074323:Alemtuzumab; D016572:Cyclosporine