Roles of IL-4 and other factors in the trichosanthin-induced ovalbumin-specific IgE response

To study the mechanism of trichosanthin (TCS)-induced ovalbumin (OVA)-specific immunoglobulin E (IgE) response in vivo.

To determine whether interleukin-4 (IL-4) was involved in TCS-induced IgE production, TCS and OVA co-immunized mice were treated with anti-IL-4 monoclonal antibodies (mAb) and OVA-specific serum IgE production was measured by enzyme-linked immunosorbent assay (ELISA). To distinguish whether recombinant IL-4 (rIL-4) was sufficient to support OVA-specific IgE response, OVA alone immunized mice were treated with rIL-4 and OVA-induced IgE production were examined by ELISA in the serum. To determine whether additional factors were involved in TCS-induced IgE response, th e kinetic expression of CD40 ligand (CD40L), tumor necrosis factor-alpha (TNF-alpha), and interleukin-13 (IL-13) were measured by semi-quantitative RT-PCR in draining mesenteric lymph node (MLN) from TCS-immunized mice.

TCS-induced OVA-specific IgE production was suppressed by anti-IL-4 antibody, whereas IL-4 alone could not induce OVA-specific IgE production. CD40L, TNF-alpha, and IL-13 all expressed high levels in MLN after both primary and secondary immune responses. Among them CD40L had the similar transient expression peak to that of IL-4.

IL-4 was indispensable for TCS-induced OVA-specific IgE production, and the other three factors examined may also be involved in, but CD40L may play a more important role.