TUMOR-NECROSIS-FACTOR-ALPHA AUGMENTS THE EXPRESSION OF FC IGE RECEPTOR (FC-EPSILON-RII/CD23) ON HUMAN MONOCYTIC CELL-LINES AND DOWN-REGULATES INTERLEUKIN-4-DRIVEN FC-EPSILON-RII EXPRESSION ON MONOCYTES

We investigated the expression of the low affinity Fc IgE receptor (FcepsilonRII/CD23) on the human monocytic cell lines U937, THP-1, Mono-Mac-6, and cultured human peripheral blood monocytes under stimulation with human tumour necrosis factor-alpha (TNF-alpha) and other cytokines. FcepsilonRII was demonstrated by flow cytometry analysis employing the anti-FcepsilonRII monoclonal antibody 3-5. TNF-alpha alone had a weak but significant stimulating effect on the FcepsilonRII expression on the cell lines U937 and THP-1, and very modestly on Mono-Mac-6 cells. TNF-alpha strongly synergized with interferon-gamma (IFN-gamma) and interleukin-4 (IL-4). IFN-alpha per se was ineffectual, but was able to increase the TNF-alpha effect. Furthermore, the action of TNF-alpha was slightly augmented by human IL-6. Similar effects were noted with TNF-beta alone or in combination with other cytokines. Interestingly, on human monocytes TNF-alpha weakly reduced the basal level of FcespsilonRII, and markedly diminished the IL-4-induced FcepsilonRII expression. Our results indicate that several cytokines may interact in a cytokine network to modulate FcepsilonRII expression on monocytic cell lines. On human blood monocytes, TNF-alpha, like IFN-gamma or IL-6, counteracts the IL-4-induced FcepsilonRII expression. These data suggest different regulatory pathways of FcepsilonRII expression on blood monocytes and myelomonocytic cell lines.