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Blood, 1 February 2001, Vol. 97, No. 3, pp. 700-707
IMMUNOBIOLOGY
The flow cytometric analysis of telomere length in
antigen-specific CD8+ T cells during acute Epstein-Barr
virus infection
Fiona J. Plunkett,
Maria
Vieira D. Soares,
Nicola Annels,
Andrew Hislop,
Kamal Ivory,
Mark Lowdell,
Mike Salmon,
Alan Rickinson, and
Arne N. Akbar
From the Department of Clinical Immunology and
Department of Haematology, Royal Free and University College Medical
School, London; Division of Immunology, Birmingham University Medical
School, Birmingham; Division of Immunology, Institute of Food Research,
Norwich Research Park, Norwich; and Department of Rheumatology, The
Medical School, University of Birmingham, Birmingham, United
Kingdom.
Acute infectious mononucleosis (AIM) induced by Epstein-Barr virus
(EBV) infection is characterized by extensive expansion of
antigen-specific CD8+ T cells. One potential consequence of
this considerable proliferative activity is telomere shortening, which
predisposes the EBV-specific cells to replicative senescence. To
investigate this, a method was developed that enables the simultaneous
identification of EBV specificity of the CD8+ T cells,
using major histocompatibility complex (MHC) class I/peptide complexes,
together with telomere length, which is determined by fluorescence in
situ hybridization. Despite the considerable expansion,
CD8+ EBV-specific T cells in patients with AIM maintain
their telomere length relative to CD8+ T cells in normal
individuals and relative to CD4+ T cells within the
patients themselves and this is associated with the induction of the
enzyme telomerase. In 4 patients who were studied up to 12 months after
resolution of AIM, telomere lengths of EBV-specific CD8+ T
cells were unchanged in 3 but shortened in one individual, who was
studied only 5 months after initial onset of infection. Substantial
telomere shortening in EBV-specific CD8+ T cells was
observed in 3 patients who were studied between 15 months and 14 years
after recovery from AIM. Thus, although telomerase activation may
preserve the replicative potential of EBV-specific cells in AIM
and after initial stages of disease resolution, the capacity of these
cells to up-regulate this enzyme after restimulation by the persisting
virus may dictate the extent of telomere maintenance in the memory
CD8+ T-cell pool over time.
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