Recent reports have demonstrated that some lymphocyte subsets are abnormal in Japanese blood donors who are seropositive for human T-lymphotropic virus type I (HTLV-I). To determine if similar changes characterize American blood donors who are seropositive for HTLV-I/II, lymphocyte subsets were measured in 42 HTLV-seropositive and 42 HTLV-seronegative blood donors. The seronegative individuals were matched by age, race, and gender to the seropositive individuals. Peripheral blood mononuclear cells were treated with a panel of 12 monoclonal antibody pairs and then analyzed by two-color flow cytometry. No significant differences were observed between the seropositive and seronegative groups with respect to the absolute number of circulating lymphocytes or the percentages of lymphocytes belonging to the subsets assessed. These subsets included B, T, CD4, and CD8 cells and subpopulations of CD4 and CD8 cells defined by the coexpression of markers that appear (CD25, HLA-DR, CD38) or disappear (Leu 8, CD45RA) after activation. These findings indicate that HTLV-seropositive persons in the American blood donor pool do not exhibit the lymphocyte subset alterations reported for HTLV-I-seropositive blood donors in Japan.

Blood↗

PubMedDate not supplied

Requirement for both the CD3/T cell receptor complex and the CD2/lymphocyte function-associated antigen-3 adhesion system in monocyte-independent T cell activation by oxidized erythrocytes.

Recent reports have shown that human T lymphocytes can be activated in vitro by desialyzed oxidized erythrocytes (DOE) in a monocyte-independent fashion. These findings suggest that, in addition to providing the activating stimulus, DOE may also fulfill accessory cell roles normally supplied by monocytes in T cell activation. DOE may thus be a useful substitute for antigen-presenting accessory cells in studies of T cell activation. This report describes experiments conducted to determine if T cell activation by DOE involves cell surface structures known to play a role in antigen-induced T cell activation. T cell stimulation by DOE was blocked by anti-CD3 monoclonal antibody, suggesting that perturbation of the CD3/T cell antigen receptor complex on T cells is required for activation. Activation was also blocked by anti-CD2 monoclonal antibody, indicating involvement of the CD2/LFA-3 adhesion system. Since DOE and monocytes both express LFA-3, the role of LFA-3 on DOE in T cell activation was assessed. DOE pretreated with anti-LFA-3 monoclonal antibody induced markedly lower levels of T cell proliferation. As further evidence for LFA-3 involvement, DOE prepared from 5 patients with paroxysmal nocturnal hemoglobinuria (PNH), known to exhibit deficient LFA-3 expression, were also deficient in T-cell stimulatory activity. These findings illustrate that T cell activation by DOE requires many of the surface structures involved in activation by antigen-bearing accessory cells, and may thus serve as a useful model for studies of T cell activation.

Antigens, CD↗