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Blood, 1 August 2001, Vol. 98, No. 3, pp. 754-761
IMMUNOBIOLOGY
Differentiation of cytomegalovirus-specific CD8+ T
cells in healthy and immunosuppressed virus carriers
Laila E. Gamadia,
Rob J. Rentenaar,
Paul A. Baars,
Ester B. M. Remmerswaal,
Sugianto Surachno,
Jan F. L. Weel,
Mireille Toebes,
Ton N. M. Schumacher,
Ineke J. M. ten
Berge, and
René A. W. van
Lier
From the Renal Transplant Unit, Department of Internal
Medicine; Clinical Immunology Laboratory and Department of
Immunobiology, Central Laboratory for Blood Transfusion and Laboratory
for Experimental and Clinical Immunology; and Department of Clinical
Virology, Academic Medical Center; and Department of Immunology, The
Netherlands Cancer Institute, Amsterdam.
During immunosuppression, cytomegalovirus (CMV) can
reactivate and cause serious clinical problems. Normally, abundant
virus replication is suppressed by immune effector mechanisms. To study the interaction between CD8+ T cells and persisting
viruses, frequencies and phenotypes of CMV-specific CD8+ T
cells were determined in healthy individuals and compared to those in
renal transplant recipients. In healthy donors, function of circulating
virus-specific CD8+ T cells, as measured by peptide-induced
interferon  (IFN-) production, but not the number of
virus-specific T cells enumerated by binding of specific tetrameric
peptide/HLA complexes, correlated with the number of CMV-specific
IFN--secreting CD4+ helper T cells. Circulating
CMV- specific CD8+ T cells did not express CCR7 and may
therefore not be able to recirculate through peripheral lymph nodes.
Based on coexpression of CD27 and CD45R0 most CMV-specific T cells in
healthy donors appeared to be memory-type cells. Remarkably,
frequencies of CMV-specific CD8+ T cells were significantly
higher in immunosuppressed individuals than in healthy donors. In
these patients CMV-specific cells predominantly had an effector
phenotype, that is,
CD45R0+CD27 CCR7 or
CD45RA+CD27CCR7 and contained
both granzyme B and perforin. Our data show that in response to
immunosuppressive medication quantitative and qualitative changes occur
in the CD8+ T-cell compartment. These adaptations may be
instrumental to maintain CMV latency.
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