Endogenous CD8+ T cell expansion during regression of monoclonal EBV- associated posttransplant lymphoproliferative disorder

Vijay P. Khatri, Robert A. Baiocchi, Ruoqi Peng, Adam R. Oberkircher, Jean M. Dolce, Pamela M. Ward, Geoffrey P. Herzig, Michael A. Caligiuri

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


There are experimental data which suggest that the primary immune effector cell responsible for maintaining immune surveillance against the outgrowth of EBV-transformed B cells in humans is the CTL, but in vivo proof of this is lacking. In this study we perform a series of cellular and molecular assays to characterize an autologous, endogenous immune response against a transplantation-associated, monoclonal, EBV+ posttransplant lymphoproliferative disorder (PTLD). Following allogeneic bone marrow transplantation, a patient developed a monoclonal PTLD of donor B cell origin. With a decrease in immune suppression, we document the emergence of endogenous, donor-derived CD3+CD8+ CTLs, followed by regression of the PTLD. The TCR Vβ repertoire went from a polyclonal pattern prior to the development of PTLD to a restricted TCR Vβ pattern during the outgrowth and regression of PTLD. Donor-derived CD3+CD8+ T lymphocytes displayed MHC class I-restricted cytolytic activity against the autologous EBV+ B cells ex vivo without additional in vitro sensitization. The striking temporal relationship between the endogenous expansion of a TCR Vβ-restricted, CD3+CD8+ population of MHC class I-restricted CTL, and the regression of an autologous monoclonal PTLD, provides direct evidence in humans that endogenous CD3+CD8+ CTLs can be responsible for effective immune surveillance against malignant transformation of EBV+ B cells.

Original languageEnglish (US)
Pages (from-to)500-506
Number of pages7
JournalJournal of Immunology
Issue number1
StatePublished - Jul 1 1999
Externally publishedYes

ASJC Scopus subject areas

  • Immunology


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