Abstract
Systemic lupus erythematosus (SLE) is a multifactorial chronic autoimmune disease, marked by the presence of autoantibodies to nuclear antigens belonging to different isotype classes. For several years, IgE antibodies have been incriminated in the development of allergic diseases and parasitic infections and different anti-IgE therapies have been developed to encounter the pathogenic role of IgE in these pathologies. Recently, multiple studies showed the presence of elevated total IgE levels and demonstrated a pathogenic role of autoreactive IgE in SLE. This review aims to summarize the findings incriminating IgE and autoreactive IgE in the pathophysiology of SLE, to describe their functional outcomes on their targeted cells as well as to discuss different IgE-related therapeutic modalities that emerged and that may be beneficial for SLE patient care.
Highlights
Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease that predominantly affects women of childbearing age
Innate cells expressing activating receptors for the Fc portion of immunoglobulins (Fc receptors) and intracellular nucleic acid receptors, such as Toll-Like Receptor (TLR) 9, TLR7 (RNA) and cyclic GMP-AMP synthase-stimulator of interferon genes (STING), are activated by circulating immune complexes (CIC) and produce pro-inflammatory cytokines amplifying autoantibody and CIC productions leading to the amplification of tissue damages [1,4]
Patients with active disease [38]. This prevalence was taking into account the four classical specificities of autoantibodies in SLE as well as three new autoantigens identified in this study (CLIP4, APEX and MPG) (Table 1) [38]
Summary
Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease that predominantly affects women of childbearing age. Antibodies 2020, 9, 69 family of B cell activating factor of the TNF family (BAFF) that stimulates B cell maturation and autoantibody production They induce type I interferon (IFN) production by dendritic cells (especially plasmacytoid dendritic cells, (pDC)) leading to an amplification of their own productions, and they allow basophil recruitment to secondary lymphoid organs where these cells amplify plasmablast number and function [5,6,7,8]. This simplified pathophysiology scheme of SLE underlines the key role of autoantibodies and CIC in flares and tissue damages occurring during disease course. As it will be discussed, the ability of IgE to regulate (directly or indirectly) the function of a number of immune cells and its strong activating features on IgE receptor-bearing cells give an immunoregulatory role to this isotype in the SLE environment that identifies it as a very promising therapeutic target
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