Campath-1G impairs human natural killer (NK) cell-mediated cytotoxicity
Campath-1 is a rat anti-human (CDw52) monoclonal antibody (MoAb) which is currently used for T cell depletion of allogeneic bone marrow and more recently peripheral blood stem cells prior to transplantation to prevent graft-versus-host disease (GVHD). In addition, in vivo Campath-1 is presently admi...
Saved in:
Published in | Bone marrow transplantation (Basingstoke) Vol. 18; no. 4; pp. 713 - 720 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Basingstoke
Nature Publishing Group
01.10.1996
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Campath-1 is a rat anti-human (CDw52) monoclonal antibody (MoAb) which is currently used for T cell depletion of allogeneic bone marrow and more recently peripheral blood stem cells prior to transplantation to prevent graft-versus-host disease (GVHD). In addition, in vivo Campath-1 is presently administered for the purpose of achieving increased immunosuppression during pre-transplant conditioning to aid in the prevention of graft rejection following T cell-depleted bone marrow transplantation (BMT). Graft-versus-leukemia (GVL) effect is an immunological effect that is of importance in controlling minimal residual disease (MRD) and reinducing remission post-BMT. It is thought that large granular lymphocytes (LGLs) and natural killer (NK) cells play a role in GVL. However, no data are available on the GVL effect post-Campath-mediated T cell-depleted allogeneic peripheral blood stem cell transplantation (alloPBSCT). In the present work, we assessed the effect of Campath-1G on the cytotoxic and proliferative capabilites of peripheral blood derived LGLs and NK cells. Campath-1G significantly inhibited binding of LGLs to tumor cells as well as resting and interleukin-2 (IL-2)-activated LGL and NK cell cytotoxic capabilites, which may be of clinical importance. |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0268-3369 1476-5365 |