Normal BALB/c mice injected i.p. with the IgE-secreting hybridomas B53 (ε,κ, anti-DNP), SE1.3 (ε,κ, anti-arsonate) or A3B1 (ε,κ, anti-TNP) were monitored for serum IgE concentrations and frequencies of splenic T lymphocytes with surface membrane receptors for the Fc portion of IgE (FcεR+ T lymphocytes). Mice with B53 or SE1.3 hybridomas initially developed high concentrations of IgE and CD8+ FcεR+ T lymphocytes, followed by a progressive decline in both serum IgE and expression of cytoplasmic ε-chains in the hybridoma cells. Serum IgE concentrations in mice with A3B1 hybridomas progressively increased without development of FcεR+ T lymphocytes nor a subsequent decline in IgE or change in cytoplasmic ε-chain expression in the A3B1 cells. An in vitro system in which the IgE-secreting hybridoma cells were cocultured with spleen cells harvested from mice with established B53 tumors was used to investigate the mechanisms involved in the inhibition of IgE production by the hybridoma cells. The results of these studies indicate: 1) the induction/upregulation of FcεR on CD8+ T lymphocytes in vivo requires factors in addition to high serum IgE concentrations; 2) in addition to CD8+ FcεR+ T lymphocytes and monocytes, another, as yet unidentified, splenic cell component appears to contribute to the process by which ε-chain expression in IgE-secreting hybridoma cells is suppressed, and 3) a hybridoma (A3B1) that fails to induce CD8+, FcεR+ T lymphocytes in vivo and is not inhibited in IgE expression in vivo, nonetheless is inhibited in IgE expression in vitro when cocultured with spleen cells from mice with B53 tumors.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Immunology|
|State||Published - 1990|