The Role of Apoptosis Proteins and Complement Components in the Etiopathogenesis of Systemic Lupus Erythematosus

Abstract

Systemic lupus erythematosus is a prototypical autoimmune disease characterized by the deregulation of T and B cells, tissue infiltration by mononuclear cells, tissue damage and the production of autoantibodies. There is a consensus that accelerated apoptosis of circulating lymphocytes and/or impaired clearance of apoptotic bodies may increase the amount of nuclear antigens presented to T lymphocytes. This process is accompanied by autoimmune responses that can lead to the development of lupus. The dysfunction of apoptosis may be a direct consequence of alterations in proteins/genes such as Fas, Bcl-2 and C1q. Increased expression of Fas antigen could intensify the exposure of hidden antigens. The overexpression of Bcl-2 protein might inhibit the removal of auto-reactive cells, and the lack of C1q could impair the clearance of self-antigens. The complete knowledge of the role of apoptosis components in the etiopathogenesis of lupus could lead to the development of new therapies targeting the apoptotic threshold, which could result in a more specific and effective disease response compared to global immunosuppression. This review summarizes the role of each component of the apoptotic process in the pathogenesis of lupus.

IL-1βand IL-6 Are Highly Expressed in RF+IgE+ Systemic Lupus Erythematous Subtype

“…All of the SLE patients in this family tested positive for IgE. Studies have reported that IgE leads to abnormal immune reaction which is followed by IgE production by activated B cells [ 32 – 34 ]. Also, activated T cells that produce IL-4, IL-5, and IL-10 provide help to B cells, which differentiate into IgE secreting plasma cells [ 33 ].…”

Apoptosis in immune-mediated diseases

“…The dysfunction due to the direct consequence of alterations in proteins/genes such as Fas, Bcl-2 and clq. [ 13 ]…”

Association between the Presence of Autoantibodies Targeting Ficolin-3 and Active Nephritis in Patients with Systemic Lupus Erythematosus

“…Recently, defects in apoptotic cells clearance leading to secondary cell necrosis and subsequent release of intracellular autoantigens has been proposed as one of the mechanisms of induction of these autoantibodies [ 3 ] [ 4 ]. According to this proposal, molecules of importance in the uptake of dying cells could have a role in host protection against autoimmune diseases, including SLE [ 5 ] [ 6 ] [ 7 ] [ 8 ].…”