Publication | Open Access
Regulation of IgE receptor expression on human peripheral blood lymphocytes by lymphocytosis promoting factor (LPF), lectins and dexamethasone.
10
Citations
32
References
1987
Year
Lymphocyte DevelopmentImmune RegulationImmunologyImmunologic MechanismFc Epsilon RImmune SystemImmunotherapyInflammationIge Receptor ExpressionM DexamethasoneSoluble FactorCell SignalingAutoimmune DiseaseImmune SurveillanceAutoimmunityCell BiologyMolecular ImmunologyImmunoglobulin EMedicine
Using a monoclonal anti-human Fc epsilon R antibody (H107), we found that lymphocytosis promoting factor (LPF), phytohaemagglutinin (PHA-P) and Concanavalin A (Con A) could induce Fc epsilon R, detected by immunofluorescence study, on normal human peripheral blood lymphocytes without IgE. The number of Fc epsilon R bearing lymphocytes was increased by stimulation with 3, 10 and 10 micrograms/ml of LPF, PHA-P and Con A, respectively, from 6.0 +/- 3.0/1000 cells to 26.0 +/- 7.9, 54.0 +/- 6.7 and 24.8 +/- 7.1/1000 cells, respectively. Although the induction of Fc epsilon R occurred neither in the separated T-enriched fraction (TEF) nor the T-depleted fraction (TDF), it recovered when the two fractions were mixed. The cell free supernatants from TEF stimulated with LPF or PHA-P could increase Fc epsilon R(+) cells in TDF, whereas those from TDF failed to increase them in TEF. The results suggest that the induction of Fc epsilon R occurs mainly on B lymphocytes by the soluble factor(s) formed by T cells stimulated with LPF or PHA-P. The induction of Fc epsilon R by stimulants was completely inhibited by 10(-6) M dexamethasone. It was demonstrated that the effects of dexamethasone on lymphocytes were dual: one was on B cells to inhibit responsive increases of Fc epsilon R, and the other was on T cells to suppress the formation of the soluble factor(s) which induced Fc epsilon R on B cells.
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