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Blood, Vol. 92 No. 7 (October 1), 1998:
pp. 2477-2483
Analysis of Major Histocompatibility Complex Class I, TAP
Expression, and LMP2 Epitope Sequence in Epstein-Barr
Virus-Positive Hodgkin's Disease
Paul G. Murray,
Christothea M. Constandinou,
John Crocker,
Lawrence S. Young, and
Richard F. Ambinder
From the CRC Institute for Cancer Studies, University of Birmingham,
Edgbaston, Birmingham; the School of Health Sciences, University of
Wolverhampton, Wolverhampton; the Department of Histopathology,
Birmingham Heartland Hospital, Birmingham, UK; and Johns Hopkins
Oncology Center, Baltimore, MD.
The Epstein-Barr virus (EBV)-encoded latent membrane proteins, LMP1
and LMP2, are consistently expressed by the malignant Hodgkin/Reed-Sternberg (HRS) cells of EBV-associated Hodgkin's disease
(HD). Cytotoxic T lymphocyte (CTL) responses to both of these proteins
have been shown in the blood of EBV-seropositive individuals, yet in HD
the apparent failure of the CTL response to eliminate HRS cells
expressing LMP1 and LMP2 in vivo has given rise to the suggestion that
HD may be characterized by the presence of defects in antigen
processing/presentation or in CTL function. This study has used
immunohistochemistry to show high-level expression of major
histocompatibility complex (MHC) class I molecules by the HRS cells of
EBV-associated HD and either low level or absence of expression of MHC
class I molecules on HRS cells of EBV-negative tumors. In addition, HRS
cells expressed high levels of transporter-associated proteins (TAP-1,
-2), irrespective of the presence of latent EBV infection. These
results suggest that global downregulation of MHC class I molecules
does not account for the apparent ability of EBV-infected HRS cells to
evade CTL responses, but may be important in the understanding of
EBV-negative disease.We have also sequenced an epitope in LMP2A
(CLGGLLTMV) that is restricted through HLA A2.1, a relatively
common allele in Caucasian populations, and showed that
this epitope is wild type in a small group of EBV-associated HLA
A2.1-positive HD tumors. This result may be relevant to proposed immunotherapeutic approaches for EBV-positive HD patients that target
CTL epitopes.
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