T-lymphocyte subpopulations in B-cell-derived non-Hodgkin's lymphomas and Hodgkin's disease
The authors used E-rosette formation and OKT3 reactivity to determine the percent of T-cells in lymph nodes involved by B-cell non-Hodgkin's lymphomas (B-NHL) and by Hodgkin's disease (HD). The percent of helper and suppressor/cytotoxic T-cells was determined by reactivity with OKT4 and OKT8, respectively. T-cells were also analyzed for two signs of activation: acquisition of Ia antigens and loss of acid a-naphthyl acetate esterase (ANAE) activity. The results were compared with those of lymph nodes exhibiting benign lymphoid hyperplasia (BLH). The percentage of T-cells ranged from 50% to 82%, mean 63 +/- 13%, in 25 cases of BLH, and from 6% to 62%, mean 23 +/- 11%, in 51 cases of B-NHL. The OKT4/T8 ratio was 1.0 to 6.2, mean 3.4 +/- 2.2, in the cases of BLH, and 0.5 to 5.1, mean 2.4 +/- 1.3, in the cases of B-NHL. There was no obvious or significant correlation between the percent of T-cells or the OKT4/T8 ratio and the surface immunoglobulin isotype expressed by the neoplastic B-cells, the morphologic category of B-NHL, or the clinical stage of disease. Activated T-cells were less than or equal to 3% in the cases of BLH and B-NHL. Fifteen lymph nodes involved by HD contained 44% to 96%, mean 74%, E+ (T) cells. Five of these 15 cases contained a significant number of E-OKT3+ cells suggesting that E-rosette formation is not always a reliable T-cell marker in HD. Three other cases contained a large number of E+OKT3- cells. The OKT4/T8 ratio ranged from 0.4 to 21.7, mean 6.7 +/- 5.3, in these cases, representing the most significant T-cell subset imbalances in this series. Large numbers of Ia+E+ and/or E+ANAE- cells, presumably activated T-cells, were present in 7 of these 15 cases of HD. These studies demonstrate the wide variation in the percent of T-cells and in the T-cell subset distribution in lymph nodes exhibiting benign lymphoid hyperplasia and in lymph nodes involved by B-cell-derived non-Hodgkin's lymphomas and Hodgkin's disease.