1. ¹Department of Pathology and Microbiology, University of Bristol, University Walk, Bristol, UK
2. ²Department of Immunology and Immunogenetics, North Bristol NHS Trust, Bristol, UK
3. ³Bone Marrow Transplant Unit, Royal Hospital for Children, Bristol, UK
4. ⁴Institute for Transfusion Sciences, National Blood Service, Bristol, UK

Correspondence: Dr RJ Garland, Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK. E-mail: R.Garland@bristol.ac.uk

Received 14 February 2005; Accepted 22 April 2005; Published online 13 June 2005.

Abstract

CAMPATH-1H (C-1H) is widely used in vivo and / or in vitro for T cell depletion in hematopoietic SCT. This humanised monoclonal antibody is specific for CD52, a marker coexpressed on the majority of human lymphocytes with CD48 and other glycosylphosphatidyl-inositol (GPI) anchored proteins. We detected CD52 / CD48 dual expression on >99% of CD3⁺ lymphocytes from normal individuals and all 15 post-SCT patients whose transplants did not utilise C-1H. By contrast, 23 / 26 patients with transplants involving C-1H (in vivo, in vitro or both) exhibited populations lacking CD52 expression that accounted for 49.7% (4.2–86.2%) of the CD3⁺ lymphocytes (median and range) in samples evaluated at a median of 2 months post-SCT. Most CD52^- cells also lacked CD48 expression. These GPI^- T cells were of either donor or mixed donor / recipient origin. They were predominant in the early months after SCT at times of profound lymphopenia and inversely correlated with the recovery of the absolute lymphocyte count (r= - 0.663, P<0.0001). The presence of CD52^- cells has been correlated previously with clinical outcome after CAMPATH therapy for both malignant and nonmalignant diseases.