Abstract
Culture of normal rat lymphocytes with rat IgE at 37°C resulted in an increase in the proportion of Fc(ε)R(+) 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 Fc(ε)R(+) cells were derived from Fc(γ)R(+) cells. Fc(ε)R(+) cells were not induced in vitro if Fc(γ)R(+) cells were depleted from normal lymphocytes before incubation with IgE. Kinetic studies for the induction of Fc(ε)R(+) cells showed that the majority of Fc(ε)R(+) cells induced in vitro bore Fc(γ)R at the early stage of differentiation. The Fc(ε)R-Fc(γ)R double-bearing cells converted to Fc(ε)R signal-bearing cells after further incubation with IgE. It was also found that induction of Fc(ε)R(+) cells by IgE was inhibited by rabbit IgG (RGG) or soluble antigen, IgG antibody complexes that have affinity for Fc(γ)R, but Fc(ε)R induced in vitro were specific for IgE. The results suggested that the binding of IgE with Fc(γ)R provided a signal to form and/or express Fc(ε)R. A high proportion of Fc(ε)R(+) 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 Fc(ε)R(+) cells does not involve recruitment of Fc(γ)R(+) cells to Fc(γ)R(+) cells; the proportion of Fc(γ)R(+) cells in a Fc(γ)R-depleted fraction was maintained by IgE. Neither RGG nor antigen-IgG antibody complexes affected the maintenance of the Fc(ε)R(+) cells by IgE. The results collectively suggested that the binding of IgE with either Fc(γ)R or Fc(ε)R(+) stimulate lymphocytes to form Fc(ε)R(+)
Original language | English (US) |
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Pages (from-to) | 2004-2010 |
Number of pages | 7 |
Journal | Journal of Immunology |
Volume | 123 |
Issue number | 5 |
State | Published - 1979 |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology