Plasmacytoid dendritic cells (pDCs) are immune cells that secrete large amounts of proinflammatory molecules, an essential function that is known to promote clearance of viral …

Dec 1, 2020 · We show that pDC numbers, TLR-mediated cytokine production, and T-cell-activating capacity are decreased prior to the onset of SLE. This impairment is unrelated to the type I IFN signature in...

Feb 16, 2016 · Plasmacytoid dendritic cells (pDCs) were considered to be the major IFNα source in systemic lupus erythematosus (SLE) but their phenotype and function in different disease status have not...

Sep 16, 2014 · Plasmacytoid dendritic cells (pDCs), a distinct subtype of dendritic cells that specialize in the secretion of high levels of IFN-α and IFN-β in response to viral nucleic acids, have...

Oct 1, 2022 · DCs play essential roles in the pathogenies of SLE, either as a “brake” to maintain immune tolerance or as an “engine” to promote autoimmunity. The variable origins, representative markers, and functions of cDCs, pDCs, and tolDCs and their therapeutic applications in …

Jun 23, 2015 · Dendritic cells (DCs) are key factors in the balance between autoimmunity and tolerance and play a role linking innate and adaptive immunity. DCs, particularly plasmacytoid DCs (pDCs), are the main source of type I interferon (IFN) cytokines, which contribute to the immunopathogenesis of SLE.

Plasmacytoid dendritic cells (pDC) may be critical for maintenance of inflammation in system lupus erythematosus (SLE) and may correlate with SLE complications, such as lupus nephritis (LN). This investigation assesses the immunophenotype of blood pDC in patients with SLE.

Jul 21, 2023 · TLR ligand-induced protein production by SLE patient peripheral mononuclear cells was abrogated by CSL362 pre-treatment including proteins over expressed in SLE patient serum. These findings implicate pDCs as key drivers in the cellular activation and production of soluble factors seen in SLE.

This study confirms pDC as the dominant source of IFN program activation found in SLE, and provides strong supportive evidence for the potential therapeutic effects of pDC depletion with CSL362 in SLE.

TLR-activated pDCs become resis-tant to glucocorticoids, underlying the limited eficacy of these drugs in SLE (Guiducci et al., 2010a). Therefore, pDCs have been proposed as a key source of aberrant IFN produc-tion and a major driver of SLE progression (Rönnblom and Alm, 2001).