scholarly journals Dysfunctional interferon-α production by peripheral plasmacytoid dendritic cells upon Toll-like receptor-9 stimulation in patients with systemic lupus erythematosus

2008 ◽  
Vol 10 (2) ◽  
pp. R29 ◽  
Author(s):  
Seung-Ki Kwok ◽  
June-Yong Lee ◽  
Se-Ho Park ◽  
Mi-La Cho ◽  
So-Youn Min ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dendritic Cells ◽  
Lupus Erythematosus ◽  
Plasmacytoid Dendritic Cells ◽  
Interferon Α ◽  
Toll Like Receptor ◽  
Systemic Lupus

scholarly journals BDCA-2, a Novel Plasmacytoid Dendritic Cell–specific Type II C-type Lectin, Mediates Antigen Capture and Is a Potent Inhibitor of Interferon α/β Induction

2001 ◽  
Vol 194 (12) ◽  
pp. 1823-1834 ◽  
Author(s):  
Andrzej Dzionek ◽  
Yoshiaki Sohma ◽  
Jun Nagafune ◽  
Marina Cella ◽  
Marco Colonna ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dendritic Cells ◽  
Monoclonal Antibodies ◽  
Dendritic Cell ◽  
Lupus Erythematosus ◽  
Plasmacytoid Dendritic Cell ◽  
Plasmacytoid Dendritic Cells ◽  
Interferon Α ◽  
Type Ii ◽  
Systemic Lupus

Plasmacytoid dendritic cells are present in lymphoid and nonlymphoid tissue and contribute substantially to both innate and adaptive immunity. Recently, we have described several monoclonal antibodies that recognize a plasmacytoid dendritic cell-specific antigen, which we have termed BDCA-2. Molecular cloning of BDCA-2 revealed that BDCA-2 is a novel type II C-type lectin, which shows 50.7% sequence identity at the amino acid level to its putative murine ortholog, the murine dendritic cell–associated C-type lectin 2. Anti–BDCA-2 monoclonal antibodies are rapidly internalized and efficiently presented to T cells, indicating that BDCA-2 could play a role in ligand internalization and presentation. Furthermore, ligation of BDCA-2 potently suppresses induction of interferon α/β production in plasmacytoid dendritic cells, presumably by a mechanism dependent on calcium mobilization and protein-tyrosine phosphorylation by src-family protein-tyrosine kinases. Inasmuch as production of interferon α/β by plasmacytoid dendritic cells is considered to be a major pathophysiological factor in systemic lupus erythematosus, triggering of BDCA-2 should be evaluated as therapeutic strategy for blocking production of interferon α/β in systemic lupus erythematosus patients.

scholarly journals Expression of the markers BDCA-2 and BDCA-4 and production of interferon-α by plasmacytoid dendritic cells in systemic lupus erythematosus

2003 ◽  
Vol 48 (9) ◽  
pp. 2524-2532 ◽  
Author(s):  
Stina Blomberg ◽  
Maija-Leena Eloranta ◽  
Mattias Magnusson ◽  
Gunnar V. Alm ◽  
Lars Rönnblom
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dendritic Cells ◽  
Lupus Erythematosus ◽  
Plasmacytoid Dendritic Cells ◽  
Interferon Α ◽  
Systemic Lupus

scholarly journals RNA sensing by conventional dendritic cells is central to the development of lupus nephritis

2015 ◽  
Vol 112 (45) ◽  
pp. E6195-E6204 ◽  
Author(s):  
Teja Celhar ◽  
Richard Hopkins ◽  
Susannah I. Thornhill ◽  
Raquel De Magalhaes ◽  
Sun-Hee Hwang ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dendritic Cells ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Moderate Increase ◽  
Rna Recognition ◽  
Toll Like Receptor ◽  
Systemic Lupus ◽  
Slow Progression ◽  
Inflammatory Milieu

Glomerulonephritis is a common and debilitating feature of systemic lupus erythematosus (SLE). The precise immune mechanisms that drive the progression from benign autoimmunity to glomerulonephritis are largely unknown. Previous investigations have shown that a moderate increase of the innate Toll-like receptor 7 (TLR7) is sufficient for the development of nephritis. In these systems normalization of B-cell TLR7 expression or temporal depletion of plasmacytoid dendritic cells (pDCs) slow progression; however, the critical cell that is responsible for driving full immunopathology remains unidentified. In this investigation we have shown that conventional DC expression of TLR7 is essential for severe autoimmunity in the Sle1Tg7 model of SLE. We show that a novel expanding CD11b+ conventional DC subpopulation dominates the infiltrating renal inflammatory milieu, localizing to the glomeruli. Moreover, exposure of human myeloid DCs to IFN-α or Flu increases TLR7 expression, suggesting they may have a role in self-RNA recognition pathways in clinical disease. To our knowledge, this study is the first to highlight the importance of conventional DC-TLR7 expression for kidney pathogenesis in a murine model of SLE.

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