CD8+ lymphocyte phenotypes were characterized during acute Epstein-Barr virus (EBV) infection, and a comparison was made to previous studies of human immunodeficiency virus (HIV). This was of interest because CD8+ cells contribute to immunologic control of both infections, but the usual outcome of EBV infection is benign, whereas untreated HIV infection is fatal. During acute EBV infection, CD8+ cells expressed elevated levels of the activation antigens CD38 and HLA-DR, similar to that during chronic HIV infection. Within 16 weeks, when EBV latency is established, CD8+ cell activation had resolved. In contrast, activation persists in HIV infection. Expression of CD38 and HLA-DR on CD8+ cells could be a marker for ongoing viral replication in both infections. Other CD8+ cell alterations observed in this study of acute EBV infection included increases in both CD62L- and CD62L+ CD8+ cells and unique kinetics in the expansion of the CD57+CD8+ cell subset.

The procedure of centrifugal elutriation was evaluated as a means of purifying large numbers of in situ lymphocytes from enzymatically disaggregated mouse mammary tumors. The eluate obtained at a flow rate of 3.0 ml/min was optimal for high levels of lymphocyte recovery with low levels of contaminating tumor cells, polymorphonuclear leukocytes, and macrophages. The majority of the tumor infiltrating lymphocytes (90%) expressed the Thy 1.2 antigen, while less than 5% possessed surface immunoglobulin. Further analysis of the T lymphocyte population was accomplished by flow cytometric analysis of in situ lymphocytes stained with fluorescein-conjugated monoclonal anti-Lyt 2 antibodies. The results of such studies reveal an increase in the levels of Lyt 2+ lymphocytes within the in situ population. To determine whether these Lyt 2+ cells were functionally active as suppressor cells, the ISL1 were mixed with spleen cells from tumor bearers and then tested for their ability to respond to mitogen and TAA-induced blast transformation of tumor-bearer spleen cells. Removal of macrophages from ISL by Sephadex G-10 columns did not alter the suppression. Treatment with monoclonal anti-Lyt 1 antibody and complement did not affect the inhibition observed. However, treatment of ISL with anti-Lyt 2+ monoclonal antibody and complement resulted in the elimination of the suppressor cell activity. We concluded that within the tumor-infiltrating lymphoreticular cells there is a population of Thy 1.2+ Lyt 2.2+ lymphocytes responsible for the suppression of mitogen and tumor-antigen-induced blastogenesis.