Influence of recombinant IL-4, IFN-alpha, and IFN-gamma on the production of human IgE-binding factor (soluble CD23).
This study documents the influence of rIL-4, IFN-gamma, and IFN-alpha on the production of IgE-BF and the expression of lymphocyte receptor for IgE or CD23 Ag (Fc epsilon R II) by human mononuclear cells. IL-4 increases the secretion of IgE-binding factor (BF) by highly purified B lymphocytes, adherent cells, and U937 monoblastic cells. The effect of IL-4 on purified B cells is augmented by costimulating the cells with F(ab')2 anti-IgM. IFN-gamma, IL-2, IL-1-alpha, or IL-1 beta and the low m.w. B cell growth factor have no effect on IgE-BF production by purified B cells even when they are used in combination with anti-IgM. Stimulation of purified T cells with IL-4 or IL-4 plus PMA leads to the production of very small amounts of IgE-BF that might well be derived from the contaminating non-T cells. IFN-gamma increases IgE-BF synthesis by unfractionated PBMC, T cell-depleted PBMC, adherent cells, and U937 cells suggesting that it induces monocytes to release IgE-BF, IFN-gamma suppresses the IL-4-induced Fc epsilon R II expression and IgE-BF production by highly purified B cells but not by PBMC or their T cell-depleted fractions. IFN-alpha inhibits IgE-BF production by IFN-gamma-stimulated PBMC and by IL-4-stimulated cells suggesting that it exerts its effect on B cells and on monocytes. Moreover IFN-alpha suppresses the IL-4-induced expression of Fc epsilon R II on B cells. Both IFN-alpha and IFN-gamma suppress the synthesis of IgE by PBMC in response to IL-4. Taken collectively the results indicate that: 1) IL-4 induces IgE-BF production by both B cells and monocytes, 2) IFN-gamma stimulates IgE-BF synthesis by monocytes but suppresses its production by IL-4-stimulated B cells, and finally 3) IFN-alpha inhibits IgE-BF synthesis in response to either IFN-gamma or IL-4.
Delespesse
G
G
University of Montreal-Notre-Dame Hospital, Quebec, Canada.
Sarfati
M
M
Peleman
R
R
D000944:Antigens, Differentiation, B-Lymphocyte / Q000096:biosynthesis* / Q000378:metabolism; D001402:B-Lymphocytes / Q000378:metabolism; D002448:Cell Adhesion; D002469:Cell Separation; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007370:Interferon Type I / Q000494:pharmacology*; D007371:Interferon-gamma / Q000494:pharmacology*; D015847:Interleukin-4; D007378:Interleukins / Q000494:pharmacology*; D008222:Lymphokines / Q000096:biosynthesis* / Q000378:metabolism; D029584:Prostatic Secretory Proteins; D011961:Receptors, Fc / Q000096:biosynthesis* / Q000378:metabolism; D017455:Receptors, IgE; D011994:Recombinant Proteins / Q000494:pharmacology*
D000944:Antigens, Differentiation, B-Lymphocyte; D007166:Immunosuppressive Agents; D007370:Interferon Type I; D007378:Interleukins; D008222:Lymphokines; D029584:Prostatic Secretory Proteins; D011961:Receptors, Fc; D017455:Receptors, IgE; D011994:Recombinant Proteins; C043076:beta-microseminoprotein; C013059:immunoglobulin-binding factors; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma