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Blood, 1 May 2002, Vol. 99, No. 9, pp. 3449-3453
TRANSPLANTATION
T-cell receptor excision circle and T-cell dynamics after
allogeneic stem cell transplantation are related to clinical
events
Mette D. Hazenberg,
Sigrid
A. Otto,
Elmar S. de
Pauw,
Helene Roelofs,
Willem E. Fibbe,
Dörte Hamann, and
Frank Miedema
From the Department of Clinical Viro-Immunology,
CLB/Sanquin, and Landsteiner Laboratory of the Academic Medical Center,
University of Amsterdam; the Department of Hematology, Leiden
University Medical Center; and the Department of Human Retrovirology,
Academic Medical Center, University of Amsterdam, The Netherlands.
It is generally believed that homeostatic responses regulate T-cell
recovery after peripheral stem cell transplantation (PSCT). We studied
in detail immune recovery in relation to T-cell depletion and clinical
events in a group of adult patients who underwent PSCT because of
hematologic malignancies. Initially, significantly increased
proportions of dividing naive, memory, and effector CD4+
and CD8+ T cells were found that readily declined, despite
still very low numbers of CD4+ and CD8+ T
cells. After PSCT, increased T-cell division rates reflected immune
activation because they were associated with episodes of infectious
disease and graft-versus-host disease (GVHD). T-cell receptor excision
circles (TRECs) were measured to monitor thymic output of naive T
cells. Mean TREC content normalized rapidly after PSCT, long before
naive T-cell numbers had significantly recovered. This is compatible
with the continuous thymic production of TREC+ naive T
cells and does not reflect homeostatic increases of thymic output. TREC
content was decreased in patients with GVHD and infectious complications, which may be explained by the dilution of TRECs resulting from increased proliferation. Combining TREC and Ki67 analysis with repopulation kinetics led to the novel insight that recovery of TREC content and increased T-cell division during immune
reconstitution after transplantation are related to clinical events
rather than to homeostatic adaptation to T-cell depletion.
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