Interleukin 5 enhances interleukin 4‐induced IgE production by normal human B cells. The role of soluble CD23 antigen

Abstract

Interleukin 4 (IL 4)-induced IgE production by peripheral blood lymphocytes and tonsil cells from normal donors was enhanced in a dose-dependent fashion by IL 5. IL 5 tested alone was not effective. The synergistic effects of IL 5 were most pronounced at suboptimal IL 4 concentrations, whereas at saturating IL 4 concentrations (200-300 U/ml), IL 5 had no effect. Interferon-gamma (IFN-gamma) and F(ab')2 fragments of monoclonal antibody 25 directed against the CD23 antigen, that blocked IL 4-induced IgE synthesis, also inhibited the production of IgE in the presence of combinations of IL 4 and IL 5, indicating that IL 5 potentiates the activation pathway through which IL 4 induces IgE production. In contrast, IL 4 (50 U/ml) blocked IL 5-induced IgA synthesis. IL 5 was ineffective in inducing the release of soluble CD23 (sCD23), but in the presence of IL 4 an enhanced release of sCD23 was observed, provided IL 4 was present at suboptimal concentrations. IFN-gamma completely blocked sCD23 release induced by IL 4 and IL 5. These results demonstrate that there is a strong quantitative correlation between sCD23 release and induction of IgE synthesis. sCD23 fraction-correlation between sCD23 release and induction of IgE synthesis. sCD23 fractionated from the Epstein-Barr virus-transformed B cell line RPMI 8866 was ineffective in inducing IgE production. However, sCD23 acted synergistically with suboptimal concentrations of IL 4. sCD23 did not modulate the IgE response at saturating concentrations of IL 4. Collectively, these data indicate that sCD23 plays an important regulatory role in the modulation of IL 4-induced IgE synthesis mediated by IFN-gamma and IL 5.

Effect of Tea Extracts and Phenolic Components on Immunoglobulin Production by Mesenteric Lymph Node Lymphocytes of Sprague-Dawley Rats.

“…Thus, class-specific regulation of lg production, the inhibition of lgE production and the stimulation of lgA production may alleviate allergic reactions. Such class-specific regulation of lg production is induced by lymphokines, such as IL-4, IL-5, IFN-c!, and IFN-y (Pene et al, 1988;Gauchat et al, 1991;Ochel et al, 1991;Rousset et al, 1991;Elson & Beagley, 1994). In addition, several biomaterials, such as bile acids, Iectins, and unsaturated fatty acids, exert a class-specific regulation of lg production of rat mesenteric lymph node (MLN) Iymphocytes (Yamada et al, 1993Lim et al, 1994a, b).…”

TNF‐α Regulates GM‐CSF‐, IL‐3‐ or M‐CSF‐Induced Fc ε RII/CD23 Gene Expression and Soluble Fc ε RII Release by Human Monocytes

“…In addition, sFc RII has been shown to suppress histamine release from basophils by inhibiting binding of IgE to Fc R on the cell surface [32]. In contrast, recombinant and purified sFc RII from Epstein-Barr virus (EBV)-transformed B cell lines have been shown to have a variety of functional activities, either alone or in synergy with cytokines, such as regulation of IgE synthesis [33][34][35][36], promotion of B cell [37] and T cell growth [38], and inhibition of monocyte migration [39]. Thus, it is possible that systemic or locally produced TNF-a regulates the immune and inflammatory response by reducing Fc RII expression on the surface of monocytes and enhancing sFc RII release from monocytes.…”

IL-5 and IL-5 receptor in asthma

“…It activates mature eosinophils and prolongs their survival in culture (Yamaguchi et al 1988)-possibly via its ability to delay apoptosis , as well as selectively enhancing eosinophil degranulation, antibody-dependent cytotoxicity and adhesion to vascular endothelium (Lopez et al 1988, Fujisawa et al 1990). IL-5 enhances the capacity of eosinophils to release LTC4 (Weller et al 1992) and also primes basophils, leading to increased histamine and LTC4 generation (Bischoff et al 1990, Laviollette et al 1995 and increases synthesis of IgM, IgA, IgE by B cells costimulated with IL-4 (Pene et al 1988, Purkerson & Isakson 1992. Although IL-5 on its own is minimally chemoattractant for eosinophils, its ability to significantly enhance the properties of stronger eosinophil chemoattractants such as Rantes and Eotaxin is probably more important , Sedgwick et al 1995, Collins et al 1995, Rothenberg et al 1996.…”