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Regulation of ige receptor expression of human peripheral blood lymphocytes by lymphocytosis promoting factor lpf lectins and dexamethasone






Clinical & Experimental Immunology 68(2): 418-426

Regulation of ige receptor expression of human peripheral blood lymphocytes by lymphocytosis promoting factor lpf lectins and dexamethasone

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 .mu.g/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 10-6M 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.


Accession: 006288633

PMID: 2958186



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