scholarly journals Activation of plasmacytoid dendritic cells and B cells with two structurally different Toll‐like receptor 7 agonists

2020 ◽  
Vol 91 (6) ◽  
Author(s):  
Olof Berggren ◽  
Pascal Pucholt ◽  
Cane Amcoff ◽  
Lars Rönnblom ◽  
Maija‐Leena Eloranta
Keyword(s):  
Dendritic Cells ◽  
B Cells ◽  
Plasmacytoid Dendritic Cells ◽  
Toll Like Receptor

scholarly journals Mice Plasmacytoid Dendritic Cells Were Activated by Lipopolysaccharides Through Toll-Like Receptor 4/Myeloid Differentiation Factor 2

2021 ◽  
Vol 12 ◽  
Author(s):  
Wei Zhang ◽  
Eun-Koung An ◽  
Juyoung Hwang ◽  
Jun-O Jin
Keyword(s):  
Dendritic Cells ◽  
B Cells ◽  
Viral Infections ◽  
Intraperitoneal Administration ◽  
Plasmacytoid Dendritic Cells ◽  
Myeloid Differentiation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Differentiation Factor ◽  
Myeloid Differentiation Factor

Plasmacytoid dendritic cells (pDCs) are known to respond to viral infections. However, the activation of pDCs by bacterial components such as lipopolysaccharides (LPS) has not been well studied. Here, we found that pDCs, conventional dendritic cells (cDCs), and B cells express high levels of toll-like receptor 4 (TLR4), a receptor for LPS. Moreover, LPS could effectively bind to not only cDCs but also pDCs and B cells. Intraperitoneal administration of LPS promoted activation of splenic pDCs and cDCs. LPS treatment led to upregulation of interferon regulatory factor 7 (IRF7) and induced production of interferon-alpha (IFN-α) in splenic pDCs. Furthermore, LPS-dependent upregulation of co-stimulatory molecules in pDCs did not require the assistance of other immune cells, such as cDCs. However, the production levels of IFN-α were decreased in cDC-depleted splenocytes, indicating that cDCs may contribute to the enhancement of IFN-α production in pDCs. Finally, we showed that activation of pDCs by LPS requires the TLR4 and myeloid differentiation factor 2 (MD2) signaling pathways. Thus, these results demonstrate that the gram-negative component LPS can directly stimulate pDCs via TLR4/MD2 stimulation in mice.

scholarly journals Dual Role of the Tyrosine Kinase Syk in Regulation of Toll-Like Receptor Signaling in Plasmacytoid Dendritic Cells

PLoS ONE ◽  
2016 ◽  
Vol 11 (6) ◽  
pp. e0156063 ◽  
Author(s):  
Besma Aouar ◽  
Denisa Kovarova ◽  
Sebastien Letard ◽  
Albert Font-Haro ◽  
Jonathan Florentin ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tyrosine Kinase ◽  
Plasmacytoid Dendritic Cells ◽  
Dual Role ◽  
Receptor Signaling ◽  
Toll Like Receptor

scholarly journals P19 TISSUE PRIMING OF PLASMACYTOID DENDRITIC CELLS ENHANCES THEIR PHAGOCYTOSIS AND LOWERS THE THRESHOLD FOR SUBSEQUENT TOLL-LIKE RECEPTOR 9 ACTIVATION

2016 ◽  
Vol 1 (4) ◽  
pp. S9-S10
Author(s):  
J. Ruben ◽  
G. Garcia-Romo ◽  
E. Breman ◽  
S. van der Kooij ◽  
A. Redeker ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Plasmacytoid Dendritic Cells ◽  
Toll Like Receptor

scholarly journals Regulation of TLR7/9 responses in plasmacytoid dendritic cells by BST2 and ILT7 receptor interaction

2009 ◽  
Vol 206 (7) ◽  
pp. 1603-1614 ◽  
Author(s):  
Wei Cao ◽  
Laura Bover ◽  
Minkwon Cho ◽  
Xiaoxia Wen ◽  
Shino Hanabuchi ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Proinflammatory Cytokines ◽  
Stromal Cell ◽  
Bone Marrow Stromal Cell ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cells ◽  
Orphan Receptor ◽  
Receptor Interaction ◽  
Type I ◽  
Toll Like Receptor

Plasmacytoid dendritic cells (pDCs) produce copious type I interferon (IFN) upon sensing nucleic acids through Toll-like receptor (TLR) 7 and TLR9. Uncontrolled pDC activation and IFN production are implicated in lymphopenia and autoimmune diseases; therefore, a mechanism controlling pDC IFN production is essential. Human pDCs specifically express an orphan receptor, immunoglobulin-like transcript 7 (ILT7). Here, we discovered an ILT7 ligand expressed by human cell lines and identified it as bone marrow stromal cell antigen 2 (BST2; CD317). BST2 directly binds to purified ILT7 protein, initiates signaling via the ILT7–FcεRIγ complex, and strongly inhibits production of IFN and proinflammatory cytokines by pDCs. Readily induced by IFN and other proinflammatory cytokines, BST2 may modulate the human pDC’s IFN responses through ILT7 in a negative feedback fashion.

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