Contribution of dendritic cells to the autoimmune pathology of systemic lupus erythematosus

Abstract

SummarySystemic lupus erythematosus (SLE) is a heterogeneous disease in which excessive inflammation, autoantibodies and complement activation lead to multisystem tissue damage. The contribution of the individual genetic composition has been extensively studied, and several susceptibility genes related to immune pathways that participate in SLE pathogenesis have been identified. It has been proposed that SLE takes place when susceptibility factors interact with environmental stimuli leading to a deregulated immune response. Experimental evidence suggests that such events are related to the failure of T-cell and B-cell suppression mediated by defects in cell signalling, immune tolerance and apoptotic mechanism promoting autoimmunity. In addition, it has been reported that dendritic cells (DCs) from SLE patients, which are crucial in the modulation of peripheral tolerance to self-antigens, show an increased ratio of activating/inhibitory receptors on their surfaces. This phenotype and an augmented expression of co-stimulatory molecules is thought to be critical for disease pathogenesis. Accordingly, tolerogenic DCs can be a potential strategy for developing antigen-specific therapies to reduce detrimental inflammation without causing systemic immunosuppression. In this review article we discuss the most relevant data relative to the contribution of DCs to the triggering of SLE.

Oral lesions as a clinical sign of systemic lupus erythematosus

“…Various organ system damage will be caused by SLE, as a consequence of the formation and deposition of autoantibodies and immune complexes. 10 The prevalence of mucosal involvement is present in approximately 9-45% of cases and accompanied by a systemic form of the disease. According to the literature, oral lesions occur more frequently in women with a female to male ratio that is 2.7 times greater.…”

Association of long noncoding RNAs expression levels and their gene polymorphisms with systemic lupus erythematosus

“…Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disease which is characterized by multiple autoantibody production, formation of immune complexes that result in multiple tissue or organ damages 1 – 3 . It has been revealed that dysregulation of the immune system, including abnormal T-cell, B-cell, and dendritic cells (DCs) responses, participates in the pathogenesis of SLE 4 – 6 . However, to date, the exact pathogenic mechanism of SLE is still unknown.…”

Analysis of the Expression and Function of Immunoglobulin-Like Transcript 4 (ILT4, LILRB2) in Dendritic Cells from Patients with Systemic Lupus Erythematosus

“…The impaired clearance of apoptotic cells observed in SLE and the opsonization of cellular apoptotic debris by autoantibodies enhances its uptake by pDC. Moreover, these apoptotic particles are able to induce the synthesis of IFN- α , which in turn favors the maturation of mDC and triggers isotype switching and autoantibody production by autoreactive B cells [ 24 – 26 ]. However, the role of ILT4 in the pathophysiology of this autoimmune disease has not been elucidated.…”