No abstract

T cell-derived supernatants (SN) that contain B cell-stimulatory factor 1 (BSF-1) and lack IL-2 promote the growth of the IL-2-dependent T cell line, HT-2, as well as three other clones or lines of T cells that can provide help to B cells. The BSF-1 purified from these SNs promotes growth of HT-2 cells approximately 50% as effectively as purified IL-2. A potential involvement for contaminating IL-2 in the BSF-1 preparations was excluded by the demonstration that anti-BSF-1 mAbs blocked the BSF-1-induced growth of HT-2 cells; in contrast, these antibodies did not block the IL-2-induced proliferation of the HT-2 cells. In addition, anti-IL-2 mAbs or anti-IL-2-R antibodies blocked the HT-2 growth-promoting activity of purified IL-2, but not BSF-1. Finally, BSF-1 promoted only a very modest growth of Con A-induced T cell blasts, and failed to induce significant growth in seven other cytotoxic, alloreactive, and long-term T cell lines. Taken together, these results indicate that in addition to its known effects on resting and LPS-stimulated B cells, BSF-1 can promote growth of certain subsets of activated T cells, in particular, those that provide help to B cells.

The regulatory influence of Interleukin 2 (IL-2) on the expression of IL-2 receptors (IL-2R) was studied using long-term cultured T-cell lines and recombinant IL-2 (r-IL-2). Three T-cell lines with different growth requirements were used as model systems: insulin-specific BK-BI-1.2 cells express IL-2R transiently after antigenic restimulation, ovalbumin-reactive BK-OVA-1R cells express IL-2R permanently, and BK-BI-2.6.C6 cells bear IL-2R constitutively but do not exhibit antigen reactivity. All three T-cell lines exhibited the property of increased IL-2R expression in the presence of r-IL-2, as tested by cytofluorometry employing monoclonal antibody AMT-13 directed at the murine IL-2R. IL-2R density was influenced selectively by r-IL-2, because the level of Thy-1.2 molecules was similar in the presence and absence of r-IL-2. With BK-BI-2.6.C6 cells, r-IL-2 was shown to upregulate high-affinity receptors. Since BK-BI-2.6.C6 and BK-OVA-1R cells were grown in the absence of feeder cells, these data show that r-IL-2 can regulate the expression of its own receptor without the participation of monokines. Results obtained with the T-cell line BK-BI-1.2, representing insulin-specific T cells with transient IL-2R expression, show that the presence of r-IL-2 did not prevent a decline in IL-2R density occurring on day 5 after antigenic stimulus. This indicates that additional mechanisms besides antigen- and IL-2-induced IL-2R upregulation are operative in controlling IL-2R density on the cell surface.