Epstein-barr virus infection abrogates the stimulatory capacity of B cells to a major histocompatibility complex class-II-restricted proliferative T-cell clone

• Published in: Human immunology 1995-02, Vol.42 (2), p.137-144
• Main Authors: van Lochern, Ellen G., Bakker, Astrid, Snijder, Simone, Aarts, Mijntje, de Gast, Gijsbert C., Goulmy, Els
• Format: Article
• Language: English
• Subjects: Antigen Presentation - immunology; B-Lymphocytes - virology; Bone Marrow Transplantation - immunology; Cell Transformation, Viral - immunology; Female; Flow Cytometry; Graft vs Host Disease - immunology; Herpesviridae Infections - immunology; Herpesvirus 4, Human - immunology; HLA-DR Antigens - genetics; Humans; Leukemia, Myeloid - immunology; Leukemia, Myeloid - therapy; Lymphocyte Activation - immunology; Lymphocyte Cooperation - immunology; Lymphocyte Culture Test, Mixed; T-Lymphocytes - immunology
• ISSN: 0198-8859; 1879-1166
• DOI: 10.1016/0198-8859(94)00091-4

After BMT, donor T cells are activated which can display GvHD as well as GvL activities. In order to study this GvL-specific T-cell response in vitro, proliferative T-cell clones from post-BMT PBMCs were generated by stimulation with a patient's leukemic cells. One CD4 + T-cell clone (designated M-33) displayed strong proliferative activity against the patient's leukemic cells but not against the patient's EBV-LCLs. The induction of proliferation, however, appeared not to be leukemia specific. Detailed analysis of the reactivity patterns revealed that T-cell clone M-33 recognizes an as yet unknown nonpolymorphic determinant in the context of self HLA-DRw52, presented by all but one type of APC. T-cell clone M-33 proliferated upon stimulation by PB-MCs, freshly isolated B cells, monocytes, dendritic cells, leukemic B cells, and nonleukemic B-cell blasts; solely in vitro EBV-transformed B cells and in vivo EBV-infected B cells failed to induce proliferation of T-cell clone M-33. Neither surface expression of MHC or accessory molecules on the EBV cells nor suppression caused by the EBV-infected cells could explain their failure to stimulate T-cell clone M-33. We therefore hypothesize that the absence of the stimulatory capacity once the B cells are vitally infected could be the result of competition for MHC class II binding of the Epstein-Barr viral peptides, thus affecting the postulated DRw52-restricted peptide for recognition by T-cell clone M-33.