Figure 1: Contribution of autoreactive IgE to SLE
pathophysiology
In SLE, plasmacytoid dendritic cells (pDC) and basophils (BAS) are
recruited to secondary lymphoid organs. There, pDC and BAS contribute to
the pathogenesis of SLE by promoting AAb production through the
production of type I interferon (IFNα/β) and IL-4, respectively. IgG
AAb, through Fcγ receptors, and IgE AAb, through FcεRI, cooperate to
facilitate the addressing of dsDNA to TLR9 in endosomal compartments of
pDC leading to increased type I IFN production. IFNα and β promote
IFN-responsive gene transcription and directly act on B cells to
facilitate maturation and differentiation into antibody-secreting cells
(plasma cells). On basophils, autoreactive IgG may engage the inhibitory
receptor for IgG, FcγRIIB, along with FcεRI engagement through
autoreactive IgE. The integrated signal leads to cytokine (IL-4)
production without inducing degranulation.