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Lymphocytes Bearing Receptors for IgE

III. Transition of FcR(+) Cells to FcR(+) Cells by IgE¹

From The Johns Hopkins University, School of Medicine, at The Good Samaritan Hospital, Baltimore, Maryland 21239

Abstract

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

A high proportion of FcR(+) 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 FcR(+) cells does not involve recruitment of FcR(+) cells to FcR(+) cells; the proportion of FcR(+) cells in a FcR-depleted fraction was maintained by IgE. Neither RGG nor antigen-IgG antibody complexes affected the maintenance of the FcR(+) cells by IgE. The results collectively suggested that the binding of IgE with either FcR or FcR stimulate lymphocytes to form FcR.

Footnotes

¹ 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.