Abstract
Systemic Lupus Erythematosus (SLE) is characterized by a wide spectrum of auto-antibodies which recognize several cellular components. The production of these self-reactive antibodies fluctuates during the course of the disease and the involvement of different antibody-secreting cell populations are considered highly relevant for the disease pathogenesis. These cells are developed and stimulated through different ways leading to the secretion of a variety of isotypes, affinities and idiotypes. Each of them has a particular mechanism of action binding to a specific antigen and recognized by distinct receptors. The effector responses triggered lead to a chronic tissue inflammation. DsDNA autoantibodies are the most studied as well as the first in being characterized for its pathogenic role in Lupus nephritis. However, others are of growing interest since they have been associated with other organ-specific damage, such as anti-NMDAR antibodies in neuropsychiatric clinical manifestations or anti-β2GP1 antibodies in vascular symptomatology. In this review, we describe the different auto-antibodies reported to be involved in SLE. How autoantibody isotypes and affinity-binding to their antigen might result in different pathogenic responses is also discussed.
Highlights
Systemic Lupus Erythematosus (SLE) is a chronic autoimmune and inflammatory syndrome whose broad etiology has been described as genetic, epigenetic, hormonal, environmental and immune-regulatory factors to be involved
The presence of autoantibodies in other inflammatory processes, the involvement of low-affinity autoantibodies in autoimmunty [16] as well as the number of self-antigens described in SLE [4], may suggest a different pathological role of autoantibodies in SLE depending on their affinity and their specificity, and may explain the wide immune-mechanisms described, further studies remain to be done
Based on their specificities, some autoantibodies can define a specific outcome of the disease and four different clusters have been proposed: (i) the double stranded DNA (dsDNA) cluster which is associated with a high incidence of renal involvement and high risk of renal damage; (ii) the Sm/RNP cluster which is associated with higher incidence of pulmonary arterial hypertension and Raynaud’s phenomenon; (iii) the anti-cardiolipin and lupus anticoagulant cluster which is associated with neuropsychiatric involvement, antiphospholipid syndrome and hemolytic anemia; and (iv) the Ro/La cluster which does not show any clinical association [52]
Summary
Systemic Lupus Erythematosus (SLE) is a chronic autoimmune and inflammatory syndrome whose broad etiology has been described as genetic, epigenetic, hormonal, environmental and immune-regulatory factors to be involved. The pathogenesis of the autoantibodies has been the focus of many studies, and, in some cases, the tissue injury and ulterior phenotypic manifestations was shown to develop as a result of autoantibody-mediated mechanisms This involves accumulation of Immune-Complexes (IC), cell. The presence of autoantibodies in other inflammatory processes (e.g., anti-dsDNA antibodies in bacterial infections [15]), the involvement of low-affinity autoantibodies in autoimmunty [16] as well as the number of self-antigens described in SLE [4], may suggest a different pathological role of autoantibodies in SLE depending on their affinity and their specificity, and may explain the wide immune-mechanisms described, further studies remain to be done. This review aims to compile the advances in understanding the functional relevance of the different autoantibody specificities, isotypes and their binding receptors in the pathogenesis of SLE
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