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 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.

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