Antibody synthesis class switching

Effective antibody synthesis and switching from IgM to the other Ig-classes requires help by Tit-cells, predominantly but not exclusive by Th-2 cells. The master cytokine responsible for a switch to IgE and thus development of an allergy is IL-4. 

Promotes antibody synthesis and Ig class switching by B cells (lgG4, IgE)... 

Lester et al. [56] showed that TSST-1 at 1 pg/ml inhibited IL-4-stimulated synthesis of IgE, but not of IgG, in PBMCs from AD patients and normal donors. Inhibition of IL-4-induced IgE production was associated with the induction of IFN-y secretion by TSST-1. This inhibitory effect was blocked by a neutralizing antibody against IFN-y (normal PBMC) or IFN-a (AD PBMC). (In normal blood, IFN-y exceeds IFN-a concentrations, whereas in AD blood, production of IFN-y by T cells is inhibited, but the production of IFN-a by monocytes is increased.) This provided the first clue that TSST-1 (at 1 pg/ml) might inhibit class switching to IgE by enhancing the synthesis of IFN-y and IFN-a. 

Substantial evidence has supported the role of IL-4 and IL-13 in the induction of IgE synthesis (194). Interleukin-4 and IL-13 are the only cytokines known that can induce IgE synthesis in vitro using the recombinant proteins (186,195). The role of IL-4 was initially identified in vitro, T-cell-derived IL-4 was able to induce IgE production by lipopolysaccharide (LPS)-stimulated murine B cells (196), and anti-IL-4/IL-4 receptor (IL-4R) antibodies inhibited IgE responses in experimental animals (197,198). The role of IL-4 in human IgE isotype switch in B cells from IgM to IgE has been established using normal unfractionated peripheral blood mononuclear cells (PBMCs) (199) and single B cells stimulated with murine and human T-cell clones (192,200). Interleukin-4 is produced by activated Th2-type CD4+ cells and Tc2 type CD8+ cells (201), mast cells, and basophils (202). Functions attributable to IL-4 include upregulation of surface CD23, MHC class II and IL-4 receptor expression on monocytes and B cells, and increased expression of VCAM-1 on endothelial cells. 

---