scholarly journals Functional dichotomy of plasmacytoid dendritic cells: Antigen‐specific activation of T cellsversusproduction of type I interferon

2008 ◽  
Vol 38 (7) ◽  
pp. 1822-1832 ◽  
Author(s):  
Peter S. Jaehn ◽  
Kurt S. Zaenker ◽  
Juergen Schmitz ◽  
Andrzej Dzionek
Keyword(s):  
Dendritic Cells ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cells ◽  
Type I

scholarly journals Type I Interferon Inhibition and Dendritic Cell Activation during Gammaherpesvirus Respiratory Infection

2007 ◽  
Vol 81 (18) ◽  
pp. 9778-9789 ◽  
Author(s):  
Janet L. Weslow-Schmidt ◽  
Nancy A. Jewell ◽  
Sara E. Mertz ◽  
J. Pedro Simas ◽  
Joan E. Durbin ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Cell Activation ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cells ◽  
The Body ◽  
Type I ◽  
Type I Ifn ◽  
Dendritic Cell Activation ◽  
Murine Gammaherpesvirus

ABSTRACT The respiratory tract is a major mucosal site for microorganism entry into the body, and type I interferon (IFN) and dendritic cells constitute a first line of defense against viral infections. We have analyzed the interaction between a model DNA virus, plasmacytoid dendritic cells, and type I IFN during lung infection of mice. Our data show that murine gammaherpesvirus 68 (γHV68) inhibits type I IFN secretion by dendritic cells and that plasmacytoid dendritic cells are necessary for conventional dendritic cell maturation in response to γHV68. Following γHV68 intranasal inoculation, the local and systemic IFN-α/β response is below detectable levels, and plasmacytoid dendritic cells are activated and recruited into the lung with a tissue distribution that differs from that of conventional dendritic cells. Our results suggest that plasmacytoid dendritic cells and type I IFN have important but independent roles during the early response to a respiratory γHV68 infection. γHV68 infection inhibits type I IFN production by dendritic cells and is a poor inducer of IFN-α/β in vivo, which may serve as an immune evasion strategy.

scholarly journals Human cytomegalovirus suppresses type I interferon secretion by plasmacytoid dendritic cells through its interleukin 10 homolog

Virology ◽  
2009 ◽  
Vol 390 (2) ◽  
pp. 330-337 ◽  
Author(s):  
W.L. William Chang ◽  
Peter A. Barry ◽  
Richard Szubin ◽  
Dai Wang ◽  
Nicole Baumgarth
Keyword(s):  
Dendritic Cells ◽  
Human Cytomegalovirus ◽  
Type I Interferon ◽  
Interleukin 10 ◽  
Plasmacytoid Dendritic Cells ◽  
Type I

scholarly journals Mesenchymal Stem Cells Alleviate Moderate-to-Severe Psoriasis by Reducing the Production of Type I Interferon (IFN-I) by Plasmacytoid Dendritic Cells (pDCs)

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Maosheng Chen ◽  
Jing Peng ◽  
Qi Xie ◽  
Na Xiao ◽  
Xian Su ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Dendritic Cells ◽  
Type I Interferon ◽  
Neutrophil Function ◽  
Plasmacytoid Dendritic Cells ◽  
Human Umbilical Cord ◽  
Therapeutic Effects ◽  
Type I ◽  
Cytokines And Chemokines

The anti-inflammatory and immunomodulatory properties of mesenchymal stem cells (MSCs) have been proposed to be involved in some autoimmune diseases and have been successfully tested in patients and mice. But their contribution to psoriasis and the underlying mechanisms involved remains elusive. Here, we explored the feasibility of using human umbilical cord-derived MSC (hUC-MSC) infusion as a therapeutic approach in an imiquimod- (IMQ-) induced psoriasis mouse model. MSC infusion were found to significantly reduce the severity and development of psoriasis, inhibit the infiltration of immune cells to the skin, and downregulate the expression of several proinflammatory cytokines and chemokines. Our results provide an explanation for the therapeutic effects of MSC infusion by first suppressing neutrophil function and then downregulating the production of type I interferon (IFN-I) by plasmacytoid dendritic cells (pDCs). Therefore, we discovered a novel mechanism of stem cell therapy for psoriasis. In summary, our results showed that MSC infusion could be an effective and safe treatment for psoriasis.

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.

scholarly journals PACSIN1 regulates the TLR7/9-mediated type I interferon response in plasmacytoid dendritic cells

2012 ◽  
Vol 42 (3) ◽  
pp. 573-579 ◽  
Author(s):  
Eiji Esashi ◽  
Musheng Bao ◽  
Yi-Hong Wang ◽  
Wei Cao ◽  
Yong-Jun Liu
Keyword(s):  
Dendritic Cells ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cells ◽  
Interferon Response ◽  
Type I

scholarly journals Wiskott-Aldrich syndrome protein–mediated actin dynamics control type-I interferon production in plasmacytoid dendritic cells

2013 ◽  
Vol 210 (2) ◽  
pp. 355-374 ◽  
Author(s):  
Francesca Prete ◽  
Marco Catucci ◽  
Mayrel Labrada ◽  
Stefania Gobessi ◽  
Maria Carmina Castiello ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Actin Polymerization ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cells ◽  
Actin Dynamics ◽  
Type I ◽  
Type I Ifn ◽  
Wiskott Aldrich Syndrome ◽  
Elevated Type ◽  
Chronic Activation

Mutations in Wiskott-Aldrich syndrome (WAS) protein (WASp), a regulator of actin dynamics in hematopoietic cells, cause WAS, an X-linked primary immunodeficiency characterized by recurrent infections and a marked predisposition to develop autoimmune disorders. The mechanisms that link actin alterations to the autoimmune phenotype are still poorly understood. We show that chronic activation of plasmacytoid dendritic cells (pDCs) and elevated type-I interferon (IFN) levels play a role in WAS autoimmunity. WAS patients display increased expression of type-I IFN genes and their inducible targets, alteration in pDCs numbers, and hyperresponsiveness to TLR9. Importantly, ablating IFN-I signaling in WASp null mice rescued chronic activation of conventional DCs, splenomegaly, and colitis. Using WASp-deficient mice, we demonstrated that WASp null pDCs are intrinsically more responsive to multimeric agonist of TLR9 and constitutively secrete type-I IFN but become progressively tolerant to further stimulation. By acute silencing of WASp and actin inhibitors, we show that WASp-mediated actin polymerization controls intracellular trafficking and compartmentalization of TLR9 ligands in pDCs restraining exaggerated activation of the TLR9–IFN-α pathway. Together, these data highlight the role of actin dynamics in pDC innate functions and imply the pDC–IFN-α axis as a player in the onset of autoimmune phenomena in WAS disease.

Sign in / Sign up

Export Citation Format

Share Document