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Apheresis‐related enrichment of CD26++ T lymphocytes: phenotypic characterization and correlation with unfavorable outcome in autologous hematopoietic progenitor cell transplantation
Author(s) -
Hildebrandt Martin,
Dijkstra Dorothea,
Gollasch Hella,
Daemen Kerstin,
StevanovicMeyer Maja,
Ludwig WolfDieter
Publication year - 2012
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1111/j.1537-2995.2011.03351.x
Subject(s) - immunology , population , transplantation , cd8 , cd34 , haematopoiesis , hematopoietic stem cell transplantation , multiple myeloma , t cell , cd38 , progenitor cell , lymphocyte , myeloid , medicine , biology , stem cell , cancer research , immune system , environmental health , genetics
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. STUDY DESIGN AND 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−). CONCLUSION: 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.