Intercellular interactions and cytokine responsiveness of peritoneal α/β and γ/δ T cells from Listeria-infected mice: Synergistic effects of interleukin 1 and 7 on γ/δ T cells

Abstract

Peritoneal γ/δ T cells from Listeria-immune mice show an enhanced potential to expand when restimulated with antigens or mitogens in vitro (see companion paper [Skeen, M. J., and H. K. Ziegler. 1993. J. Exp. Med. 178:971]). When cocultured with peritoneal α/β T cells, the γ/δ T cell population expanded preferentially even when the in vitro stimulus was specific for the α/β T cell population. Purified γ/δ T cells did not respond to α/β T cell-specific stimuli. If isolated T cell subsets were recombined in cell mixing experiments, the resulting proliferative response was greater than additive. Irradiated α/β T cells could enhance the proliferation of responding γ/δ T cells, but the effect was unidirectional; i.e., irradiated γ/δ T cells did not stimulate responding γ/δ T cells. This effect appeared to be cytokine mediated and did not require cell-cell contact. Both recombinant interleukin 2 (rIL-2) and rIL-7 could support the expansion of the γ/δ T cells, while rIL-7 was only minimally stimulatory for the α/β T cells. The magnitude of the response by γ/δ T cells to rIL-7 exceeded the response to other in vitro stimuli, including immobilized anti-T cell receptor monoclonal antibody, and was 50-100-fold greater than the α/β T cell response to IL-7. This unique sensitivity of γ/δ T cells to IL-7 was strongly enhanced by the presence of accessory cells. These cells could be replaced by rIL-1, establishing a synergy for IL-1 and IL-7 as factors that could uniquely stimulate this γ/δ T cell population. Isolated peritoneal γ/δ T cells from Listeria-immune mice react to heat-killed Listeria preparations in the presence of macrophage accessory cells in a non-H-2-restricted manner. Considered collectively, these results suggest a potential mechanism by which γ/δ T cells can predominate in epithelial tissues and at sites of infection.