Abstract.
Background: All-trans retinoic acid (ATRA) inhibits IgE synthesis from anti-CD40 plus IL-4 stimulated human B lymphocytes.
Objective: To study the underlying mechanisms, we examined here molecules which are known to have an impact on IgE production, namely CD23, CD54 and IL-6.
Methods: Human anti-CD40 plus IL-4 stimulated B cells were cultured in the absence and presence of ATRA (10−6–10−10 M). ELISAs were performed to determine soluble (s) CD23 and sCD54, IL-6 and IgE-levels. CD23 and CD54 surface expression were determined by flow cytometric analysis. Semiquantitative-RT-PCR was employed to analyse IL-6, CD23 and CD54 mRNA expression.
Results: ATRA induced a dose-dependent increase of percent CD23 (3.4 fold) or CD54 (1.6 fold) positive B cells. At the mRNA level, this was reflected by a modest increase of CD54 mRNA (46.5 ± 15.8%) only. By contrast, levels of sCD54 were decreased dose-dependently in the presence of ATRA (56.6 ± 7.6%). Cytokine analysis showed that IL-6 secretion was significantly inhibited by ATRA (53.6 ± 0.6%) and also IL-6 mRNA synthesis was reduced (66.3 ± 11.6%). The observed inhibition of IgE production mediated by ATRA was significantly reversed to 90.5 ± 12% by the addition of 100 pg/mL recombinant IL-6.
Conclusions: ATRA interferes through several pathways with the anti-CD40 plus IL-4 mediated B cell activation, namely IL-6, CD23 and CD54.
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Received 8 June 2004; returned for revision 19 July 2004; accepted by M. J. Parnham 5 November 2004
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Scheffel, F., Heine, G., Henz, B.M. et al. Retinoic acid inhibits CD40 plus IL-4 mediated IgE production through alterations of sCD23, sCD54 and IL-6 production. Inflamm. res. 54, 113–118 (2005). https://doi.org/10.1007/s00011-004-1331-8
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DOI: https://doi.org/10.1007/s00011-004-1331-8