Premium
Anti‐CD52 antibody, alemtuzumab, binds to Langerhans cells in Langerhans cell histiocytosis
Author(s) -
Jordan Michael B.,
McClain Kenneth L.,
Yan Xiaotian,
Hicks John,
Jaffe Ronald
Publication year - 2005
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.20181
Subject(s) - cd52 , alemtuzumab , langerhans cell histiocytosis , medicine , histiocyte , immunohistochemistry , antibody , histiocytosis , immunology , pathology , cd20 , disease
Abstract Background The humanized anti‐CD52 monoclonal antibody, alemtuzumab (or Campath‐1H), has been shown to potently deplete lymphocytes in human patients. It has been used to successfully treat graft versus host disease and chronic lymphocytic leukemia (CLL). CD52 is expressed on normal lymphocytes, monocytes, and some dendritic cell subsets. However, normal Langerhans cells (LC's) in the skin do not bind alemtuzumab. We sought to determine whether the pathologic LC's of Langerhans cell histiocytosis (LCH) express CD52 and thus could be targeted by this antibody. Methods Immunohistochemistry was performed on both frozen and fixed/paraffin‐embedded tissue specimens using either Campath‐1G (the parental rat isotype) or Campath‐1H (the humanized version of Campath in clinical use). Results Both Campath‐1H and Campath‐1G were found to bind to the pathologic LC's in LCH, but not the normal LC's of skin. Specific staining was demonstrated in all (13 of 13) LCH specimens examined, though staining was somewhat variable among specimens, and tended to be weaker in paraffin‐embedded specimens. Conclusions Expression of CD52 by the pathologic LC's seen in LCH suggests that alemtuzumab may represent a new, targeted therapy for this disease. Such therapy is particularly needed for patients with refractory, high‐risk disease. Further investigation of the possible clinical use of this antibody in these patients is warranted. © 2004 Wiley‐Liss, Inc.