title: Apheresis-related enrichment of CD26++ T lymphocytes: phenotypic characterization and correlation with unfavorable outcome in autologous hematopoietic progenitor cell transplantation.
abstract: BACKGROUND
  The lymphocyte surface glycoprotein CD26 anchors adenosine deaminase to the lymphocyte surface and possesses dipeptidyl peptidase IV activity. A distinct subset of CD26++ lymphocytes in autologous hematopoietic progenitor cell transplants (HPCTs) was investigated with regard to clinical outcome after autologous HPCT. The phenotype of these cells was characterized in more detail.
  
  
  METHODS
  Forty-two eligible patients (multiple myeloma, n = 31; Hodgkin's disease, n = 3; non-Hodgkin's lymphoma, n = 6; peripheral neuroectodermal tumor, n = 1; acute myeloid leukemia, n = 1) were included in a retrospective analysis. Distinct cellular subsets, including CD26+/- and CD26++ subpopulations, were analyzed for correlations with kinetics of engraftment, progression-free survival, and overall survival.
  
  
  RESULTS
  The numbers of CD26++ T lymphocytes in the autograft correlated inversely with progression-free survival (p = 0.013). CD26++ T lymphocytes transfused per kg of body weight were predictive for the occurrence of disease progression or relapse (p = 0.006). Importantly, the numbers of CD26++ cells showed a highly variable degree of enrichment in the autograft, but no significant variations in the peripheral blood before apheresis. The characterization of CD26++ cells revealed that CD26++/CD8+ cells form a homogeneous population with a distinct T memory cell phenotype (CD45RO+, CD161++, interleukin-18Rα++, CCR7-).
  
  
  CONCLUSIONS
  CD26++ lymphocytes define a discrete phenotype of T memory cells with known chemoresistance and T-cell-repopulating capacity. Their enrichment during apheresis and corresponding depletion from the circulation are associated with an adverse outcome in autologous HPCT.
authors.affiliation: GMP Development Unit, Integrated Research and Treatment Center Transplantation (IFB-Tx), Medical School Hannover, Hannover, Germany. martin.hildebrandt@lrz.tu-muenchen.de
authors.forename: Martin
authors.initials: M
authors.lastname: Hildebrandt
authors.forename: Dorothea
authors.initials: D
authors.lastname: Dijkstra
authors.forename: Hella
authors.initials: H
authors.lastname: Gollasch
authors.forename: Kerstin
authors.initials: K
authors.lastname: Daemen
authors.forename: Maja
authors.initials: M
authors.lastname: Stevanovic-Meyer
authors.forename: Wolf-Dieter
authors.initials: WD
authors.lastname: Ludwig
mesh_terms: D001781:Blood Component Removal; D018819:Dipeptidyl Peptidase 4 / Q000032:analysis*; D006410:Hematopoiesis; D018380:Hematopoietic Stem Cell Transplantation / Q000009:adverse effects / Q000401:mortality; D006801:Humans; D016130:Immunophenotyping; D010641:Phenotype; D013601:T-Lymphocytes / Q000276:immunology*; D014182:Transplantation, Autologous
chemical_list: C042807:DPP4 protein, human; D018819:Dipeptidyl Peptidase 4