Abstract
System lupus erythematosus (SLE) is a multifactorial systemic autoimmune disease with a wide variety of presenting features. SLE is believed to result from dysregulated immune responses, loss of tolerance of CD4 T cells and B cells to ubiquitous self-antigens, and the subsequent production of anti-nuclear and other autoreactive antibodies. Recent research has associated lupus development with changes in the dendritic cell (DC) compartment, including altered DC subset frequency and localization, overactivation of mDCs and pDCs, and functional defects in DCs. Here we discuss the current knowledge on the role of DC dysfunction in SLE pathogenesis, with the focus on DCs as targets for interventional therapies.
Highlights
Systemic lupus erythematosus is a chronic autoimmune inflammatory disease that affects multiple organ systems, prototypically characterized by high levels of circulating autoantibodies and glomerulonephritis
Inflammatory dendritic cell (DC) have been suggested to originate from classic CD14+ blood monocytes under inflammatory conditions
Mouse models have several advantages: (i) the relative homology between human and mouse DCs, (ii) the opportunity to genetically or pharmacologically eliminate specific DC populations during specific stages of disease, (iii) access to all target tissues for the assessment of tissue associated or infiltrating DCs, (iv) the opportunity to assess the effects of common treatments on the parameters, and (v) a plethora of biological and pharmacological tools to dissect the relative contribution of specific molecules and mediators to the development and progression of disease
Summary
Systemic lupus erythematosus is a chronic autoimmune inflammatory disease that affects multiple organ systems, prototypically characterized by high levels of circulating autoantibodies and glomerulonephritis. SLE is believed to result from dysregulated immune responses, loss of tolerance of CD4 T cells and B cells to ubiquitous self-antigens, and the subsequent production of antinuclear and other autoreactive antibodies This dysregulation is associated with high serum levels of type I IFN, observed in greater than 70% of patients [16, 17]. Current “standard of care” treatments encompass high-dose corticosteroids, antimalarials, and immunosuppressive drugs that are associated with significant adverse side effects. As these treatments suppress symptoms and do not cure the disease, new therapies are needed. Full dissection of the relative contribution of the causes and the consequences of the dysfunctionality in the different DC subpopulations is needed to understand the processes that govern SLE development, progression, remission, and relapses, in order to design interventional treatments that have the potential to redirect the immune system and eventually lead to a cure for this disease
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