7 April 2014, by DE MASSON A. & RAM-WOLFF C. & BAGOT M.


Alemtuzumab (Campath-1H, Mabcampath®, Campath®, Lemtrada®) is a humanised monoclonal IgG antibody that recognizes a specific glycoprotein (CD52) expressed at the surface of virtually all T and B lymphocytes and, to a lesser extent, of NK lymphocytes, monocytes and macrophages [1]. Campath® causes lyses of target cells expressing CD52, essentially through antibody-dependent cell cytotoxicity (ADCC) mediated by NK cells and neutrophils [2-5] and through complement-dependent cytotoxicity [6]. Alemtuzumab therefore leads to depletion of tumour B and T lymphocytes expressing CD52 and to severe and sometimes persistent lymphopenia [7]. The efficacy of alemtuzumab in inducing NK-mediated ADCC has been demonstrated in vitro in blood samples from Sézary syndrome (SS) patients [2]. It is less effective against mycosis fungoides (MF) [3, 8-10]. Another study has suggested that the lesser efficacy against MF could be due to an absence of recirculation of MF cells in peripheral blood as opposed to SS tumour cells. Mycosis fungoides tumour cells appear to express skin-homing molecules and therefore are not affected by alemtuzumab-related ADCC because of the absence of NK effector cells or neutrophil in the skin as opposed to in the peripheral blood [3].

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