Culture of normal rat lymphocytes with rat IgE at 37°C resulted in an increase in the proportion of FcεR(+) cells. In agreement with this finding, the ability of normal lymphocytes to bind 125I-IgE markedly increased after overnight incubation with IgE. Evidence was obtained that FcεR(+) cells were derived from FcγR(+) cells. FcεR(+) cells were not induced in vitro if FcγR(+) cells were depleted from normal lymphocytes before incubation with IgE. Kinetic studies for the induction of FcεR(+) cells showed that the majority of FcεR(+) cells induced in vitro bore FcγR at the early stage of differentiation. The FcεR-FcγR double-bearing cells converted to FcεR signal-bearing cells after further incubation with IgE. It was also found that induction of FcεR(+) cells by IgE was inhibited by rabbit IgG (RGG) or soluble antigen—IgG antibody complexes that have affinity for FcγR, but FcεR induced in vitro were specific for IgE. The results suggested that the binding of IgE with FcγR provided a signal to form and/or express FcεR.

A high proportion of FcεR(+) cells in the mesenteric lymph nodes from rats infected with Nippostrongylus brasiliensis was maintained if the lymphocytes were cultured in IgE, whereas the proportion markedly diminished if the cells were kept overnight in IgE-free medium. Evidence was obtained that the maintenance in the proportion of FcεR(+) cells does not involve recruitment of FcγR(+) cells to FcεR(+) cells; the proportion of FcεR(+) cells in a FcγR-depleted fraction was maintained by IgE. Neither RGG nor antigen-IgG antibody complexes affected the maintenance of the FcεR(+) cells by IgE. The results collectively suggested that the binding of IgE with either FcγR or FcεR stimulate lymphocytes to form FcεR.


This work was supported by Research Grants AI-10060 from the United States Public Health Service and PCM-78-10475 from the National Science Foundation. This paper is publication No. 361 from the O'Neill Laboratories at the Good Samaritan Hospital.

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