Abstract
Dendritic cells (DC) play an important role in the pathogenesis of systemic lupus erythematosus (SLE), an autoimmune disease with multiple tissue manifestations. In this review, we summarize recent studies on the roles of conventional DC and plasmacytoid DC in the development of both murine lupus and human SLE. In the past decade, studies using selective DC depletions have demonstrated critical roles of DC in lupus progression. Comprehensive in vitro and in vivo studies suggest activation of DC by self-antigens in lupus pathogenesis, followed by breakdown of immune tolerance to self. Potential treatment strategies targeting DC have been developed. However, many questions remain regarding the mechanisms by which DC modulate lupus pathogenesis that require further investigations.
Highlights
Systemic lupus erythematosus (SLE) is an autoimmune disease that causes damage of multiple organs [1]
The levels of anti-LL37 and anti-HNP antibodies in the patient sera are increased, which, when ligated with transmembrane expressed LL37 and HNP, respectively, can trigger the release of neutrophil extracellular traps (NETs) by neutrophils. These results suggest that a positive feedback loop between NETs release by neutrophils and interferon α (IFNα) production by plasmacytoid DC (pDC) may initiate and/or promote lupus development in SLE patients
It is possible that pDC in SLE patients and lupus-prone mice can still produce a normal level of IFNα through the TLR7 pathway
Summary
Systemic lupus erythematosus (SLE) is an autoimmune disease that causes damage of multiple organs [1]. DC were discovered as the professional antigen-presenting cells (APC) with a primary function of priming naıve T cell activation [7]. Since their discovery, our understanding of how DC contribute to immune responses has much expanded, and DC have been divided into many subpopulations with distinct phenotypes and functions [8]. CDC are professional APC that prime naıve T cells upon antigen uptake and maturation induced by appropriate maturation signals (e.g., upon TLR ligation). PDC can upregulate MHC-II upon activation and act like cDC to activate T cells [10] Both cDC and pDC are important for immune tolerance to self [8]. We summarize recent results obtained from studies of SLE patients and lupus-prone mice on the roles of cDC and pDC in lupus development
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