Immune status following alemtuzumab treatment in human CD52 transgenic mice

被引：49

作者：

Turner, Michael J. ^{[1
]}

LaMorte, Michael J. ^{[1
]}

Chretien, Nathalie ^{[1
]}

Havari, Evis ^{[1
]}

Roberts, Bruce L. ^{[1
]}

Kaplan, Johanne M. ^{[1
]}

Siders, William M. ^{[1
]}

机构：

[1] Genzyme Corp, Neuroimmunol Res, Framingham, MA 01701 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2013年 / 261卷 / 1-2期

关键词：

Alemtuzumab; Immune status; CD52; Multiple sclerosis; THERAPEUTIC LYMPHOCYTE DEPLETION; CONTROLLED PHASE-3 TRIAL; MULTIPLE-SCLEROSIS; T-CELLS; CAMPATH-1H; DISEASE;

D O I：

10.1016/j.jneuroim.2013.04.018

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Alemtuzumab is a monoclonal antibody against the CD52 antigen present at high levels on the surface of lymphocytes. While treatment of multiple sclerosis patients with alemtuzumab results in marked depletion of lymphocytes from the circulation, it has not been associated with a high incidence of serious infections. In a human CD52 transgenic mouse, alemtuzumab treatment showed minimal impact on the number and function of innate immune cells. A transient decrease in primary adaptive immune responses was observed post-alemtuzumab but there was little effect on memory responses. These results potentially help explain the level of immunocompetence observed in alemtuzumab-treated MS patients. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved.

引用

页码：29 / 36

页数：8

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