title: The effects of CAMPATH-1H on cell viability do not correlate to the CD52 density on the cell surface.
abstract: Graft versus host disease (GvHD) is one of the main complications after hematological stem cell transplantation (HSCT). CAMPATH-1H is used in the pre-transplant conditioning regimen to effectively reduce GvHD by targeting CD52 antigens on T cells resulting in their depletion. Information regarding CD52 expression and the effects of CAMPATH-1H on immune cells is scant and limited to peripheral blood (PB) T and B cells. To date, the effects of CAMPATH-1H on cord blood (CB) cells has not been studied. Here we aimed to analyze CD52 expression and the effects of CAMPATH-1H on fresh or frozen, resting or activated, PB mononuclear cells (PBMC) and CB mononuclear cells (CBMC). In resting state, CD52 expression was higher in CB than PB T cell subsets (653.66 ± 26.68 vs 453.32 ± 19.2) and B cells (622.2±20.65 vs 612.0 ± 9.101) except for natural killer (NK) cells where CD52 levels were higher in PB (421.0 ± 9.857) than CB (334.3 ± 9.559). In contrast, CD52 levels were comparable across all cell types after activation. CAMPATH-1H depleted resting cells more effectively than activated cells with approximately 80-95% of apoptosis observed with low levels of necrosis. There was no direct correlation between cell surface CD52 density and depleting effects of CAMPATH-1H. In addition, no difference in cell viability was noted when different concentrations of CAMPATH-1H were used. CD52 was not expressed on HSC but began to be expressed as the cells differentiate, implying that CAMPATH-1H could potentially affect HSC differentiation and proliferation. Our study provides insightful information, which contributes to the better understanding in the use of CAMPATH-1H as part of the conditioning regime in HSCT.
authors: University College London, Cancer Institute, London, United Kingdom; Anthony Nolan Research Institute, London, United Kingdom.
authors: Fuiyee
authors: F
authors: Lee
authors: University College London, Cancer Institute, London, United Kingdom; Anthony Nolan Research Institute, London, United Kingdom.
authors: Martha
authors: M
authors: Luevano
authors: University College London, Cancer Institute, London, United Kingdom; Anthony Nolan Research Institute, London, United Kingdom; Great Ormond Street Hospital for Children NHS, London, United Kingdom.
authors: Paul
authors: P
authors: Veys
authors: University College London, Cancer Institute, London, United Kingdom.
authors: Kwee
authors: K
authors: Yong
authors: University College London, Cancer Institute, London, United Kingdom; Anthony Nolan Research Institute, London, United Kingdom.
authors: Alejandro
authors: A
authors: Madrigal
authors: University College London, Cancer Institute, London, United Kingdom; Anthony Nolan Research Institute, London, United Kingdom; Royal Marsden NHS Foundation Trust, Sutton, United Kingdom.
authors: Bronwen E
authors: BE
authors: Shaw
authors: University College London, Cancer Institute, London, United Kingdom; Anthony Nolan Research Institute, London, United Kingdom.
authors: Aurore
authors: A
authors: Saudemont
mesh_terms: D000074323:Alemtuzumab; D061067:Antibodies, Monoclonal, Humanized / Q000494:pharmacology*; D015703:Antigens, CD / Q000032:analysis* / Q000276:immunology; D000951:Antigens, Neoplasm / Q000032:analysis* / Q000276:immunology; D000970:Antineoplastic Agents / Q000494:pharmacology*; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology; D000074301:CD52 Antigen; D002469:Cell Separation; D002470:Cell Survival / Q000187:drug effects*; D006023:Glycoproteins / Q000032:analysis* / Q000276:immunology; D006801:Humans; D007694:Killer Cells, Natural / Q000187:drug effects / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000276:immunology
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D015703:Antigens, CD; D000951:Antigens, Neoplasm; D000970:Antineoplastic Agents; D000074301:CD52 Antigen; C000613862:CD52 protein, human; D006023:Glycoproteins; D000074323:Alemtuzumab