Interleukin 4 (BSF-1) induces growth in resting murine CD8 T cells triggered via cross-linking of T3 cell surface structures

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Abstract
To analyze the role of interleukin 4 (IL4, BSF‐1) during primary activation of resting (high‐density) murine CD8 T cells, a model system was used which bypasses antigen‐presenting cells by the use of anti‐T3 monoclonal antibodies immobilized on Sepharose beads. In high, but not in low cell density cultures, IL4 alone induced cell growth. In low cell density cultures, further to T3 cross‐linking a soluble macrophage product was required as co‐stimulator to induce sensitivity to IL4. This co‐stimulator activity was unrelated to recombinant (r)IL1, rIL6 and rTNF‐α (tumor necrosis factor α). In primary CD8 T cell responses rIL4‐driven growth was about half of that induced by rIL2, and not inhibitable by anti‐IL 2 receptor antibodies. Higher concentrations of IL4 down‐regulated cell proliferation. In the course of IL4‐driven growth, the proliferating cells acquired sensitivitiy to the growth‐promoting effect of IL2. Activated CD4 or CD8 T cells were found to be equally sensitive to the IL4 and IL2‐driven growth pathway. Taken together, these results define a physiologic role of IL4 as growth factor during primary activation of resting CD8 T cells and thus extend the spectrum of target cells for IL4.