scholarly journals Clonal Type I Interferon–producing and Dendritic Cell Precursors Are Contained in Both Human Lymphoid and Myeloid Progenitor Populations

2004 ◽  
Vol 200 (11) ◽  
pp. 1519-1524 ◽  
Author(s):  
Laurie Chicha ◽  
David Jarrossay ◽  
Markus G. Manz

Because of different cytokine responsiveness, surface receptor, and transcription factor expression, human CD11c− natural type I interferon–producing cells (IPCs) and CD11c+ dendritic cells were thought to derive through lymphoid and myeloid hematopoietic developmental pathways, respectively. To directly test this hypothesis, we used an in vitro assay allowing simultaneous IPC, dendritic cell, and B cell development and we tested lymphoid and myeloid committed hematopoietic progenitor cells for their developmental capacity. Lymphoid and common myeloid and granulocyte/macrophage progenitors were capable of developing into both functional IPCs, expressing gene transcripts thought to be associated with lymphoid lineage development, and into dendritic cells. However, clonal progenitors for both populations were about fivefold more frequent within myeloid committed progenitor cells. Thus, in humans as in mice, natural IPC and dendritic cell development robustly segregates with myeloid differentiation. This would fit with natural interferon type I–producing cell and dendritic cell activity in innate immunity, the evolutionary older arm of the cellular immune system.

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 ◽  
...  

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.


2013 ◽  
Vol 88 (2) ◽  
pp. 859-867 ◽  
Author(s):  
T. Rodriguez-Calvo ◽  
J.-M. Rojas ◽  
V. Martin ◽  
N. Sevilla

2013 ◽  
Vol 210 (12) ◽  
pp. 2515-2522 ◽  
Author(s):  
Yi-Ling Chen ◽  
Ting-Ting Chen ◽  
Li-Mei Pai ◽  
Joanna Wesoly ◽  
Hans A.R. Bluyssen ◽  
...  

During infections and inflammation, plasmacytoid dendritic cells (pDCs) are the most potent type I interferon (IFN-I)–producing cells. However, the developmental origin of pDCs and the signals dictating pDC generation remain incompletely understood. Here, we report a synergistic role for IFN-I and Flt3 ligand (FL) in pDC development from common lymphoid progenitors (CLPs). Both conventional DCs (cDCs) and pDCs were generated from CLPs in response to FL, whereas pDC generation required higher concentrations of FL and concurrent IFN-I signaling. An absence of IFN-I receptor, impairment of IFN-I signaling, or neutralization of IFN-I significantly impeded pDC development from CLPs. Furthermore, FL induced IFN-I expression in CLPs, which in turn induced Flt3 up-regulation that facilitated survival and proliferation of CLPs, as well as their differentiation into pDCs. Collectively, these results define a critical role for the FL/IFN-I/Flt3 axis in pDC differentiation from CLPs.


2010 ◽  
Vol 84 (9) ◽  
pp. 4845-4850 ◽  
Author(s):  
Juan R. Rodriguez-Madoz ◽  
Dabeiba Bernal-Rubio ◽  
Dorota Kaminski ◽  
Kelley Boyd ◽  
Ana Fernandez-Sesma

ABSTRACT Dengue virus (DENV) infects human immune cells in vitro and likely infects dendritic cells (DCs) in vivo. DENV-2 productive infection induces activation and release of high levels of chemokines and proinflammatory cytokines in monocyte-derived DCs (moDCs), with the notable exception of alpha/beta interferon (IFN-α/β). Interestingly, DENV-2-infected moDCs fail to prime T cells, most likely due to the lack of IFN-α/β released by moDCs, since this effect was reversed by addition of exogenous IFN-β. Together, our data show that inhibition of IFN-α/β production by DENV in primary human moDCs is a novel mechanism of immune evasion.


2007 ◽  
Vol 1106 (1) ◽  
pp. 253-261 ◽  
Author(s):  
N. ONAI ◽  
A. OBATA-ONAI ◽  
M. A. SCHMID ◽  
M. G. MANZ

Sign in / Sign up

Export Citation Format

Share Document