Purified excretory-secretory component of filarial parasite enhances Fc epsilon RII/CD23 expression on human splenic B and T cells and IgE synthesis while potentiating T-helper type 2-related cytokine generation from T cells.

The CD23-bearing cells are known to be involved in multiple biological activities, including IgE synthesis and IgE-dependent cytotoxicity to parasites. The factors that regulate interleukin-4 (IL-4)-induced IgE synthesis in helminthic infection were analysed by using an excretory-secretory component (ESC) of Dirofilaria immitis (DI). Human splenic B and T cells significantly enhanced the expression of low-affinity Fc receptors for IgE (Fc epsilon RII/CD23) by stimulation with ESC, either acting alone or in synergy with IL-4. On B cells, ESC potentiated the CD23 expression in synergy with IL-4, whereas ESC alone was unable to modulate CD23 expression. In contrast, ESC directly induced CD23 expression on T cells by acting alone and no further enhancement was observed in the presence of IL-4. Furthermore, IL-4-induced IgE synthesis by splenic mononuclear cells (SMNC) was greatly enhanced in the presence of ESC. Of particular interest, T cells primed by ESC significantly produced a set of cytokines including IL-3, IL-4, IL-5 and IL-6. Inasmuch, IL-4-induced IgE synthesis in helminthic infection may be selectively modulated by parasite protein(s) acting on the generation of T-helper type 2 (Th2)-related cytokines.