Limited humoral immunoglobulin E memory influences serum immunoglobulin E levels in blood.

The switch of B cells expressing membrane-bound Igs, which serve as antigen receptors, to antibody-secreting plasmablasts and finally to non-dividing, long-lived plasma cells (PCs) lacking an antigen receptor, marks the terminal differentiation of a B cell. Antibody-secreting PCs represent the key cell type for the maintenance of a proactive humoral immunological memory. Although some populations of long-lived PCs persist in the spleen, most of them return to their 'place of birth' and travel to the bone marrow or invade inflamed tissues, where they survive up to several months in survival niches as resident, immobile cells. Existing data strongly support the notion that isotype-specific receptor signalling influences the migration behaviour of plasmablasts to the bone marrow. The recent observation in the murine system that the immigration of plasmablasts and the final differentiation to long-lived PCs in the bone marrow is dependent on the expressed B-cell isotype and the related expression of chemokine receptors leads to the conclusion that during a T-helper type 2 (Th2)-mediated immune response in wild type mice, IgE plasmablasts do not have the same chance to contribute to long-lived PC memory as IgG1 plasmablasts. The overall limited humoral IgE memory additionally restricts the quantity of IgE Igs in the serum.