scholarly journals HIV-1 Nef Protein Affects Cytokine and Extracellular Vesicles Production in the GEN2.2 Plasmacytoid Dendritic Cell Line

Viruses ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 74
Author(s):  
Alessandra Aiello ◽  
Flavia Giannessi ◽  
Zulema Antonia Percario ◽  
Katia Fecchi ◽  
Claudia Arenaccio ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Cell Line ◽  
Plasmacytoid Dendritic Cell ◽  
Cell Subset ◽  
Extracellular Vesicle ◽  
Type I ◽  
Dendritic Cell Subset ◽  
System A ◽  
New Information ◽  
Tnf Α

Plasmacytoid dendritic cells (pDCs) are a unique dendritic cell subset specialized in type I interferon production, whose role in Human Immunodeficiency Virus (HIV) infection and pathogenesis is complex and not yet well defined. Considering the crucial role of the accessory protein Nef in HIV pathogenicity, possible alterations in intracellular signalling and extracellular vesicle (EV) release induced by exogenous Nef on uninfected pDCs have been investigated. As an experimental model system, a human plasmacytoid dendritic cell line, GEN2.2, stimulated with a myristoylated recombinant NefSF2 protein was employed. In GEN2.2 cells, Nef treatment induced the tyrosine phosphorylation of STAT-1 and STAT-2 and the production of a set of cytokines, chemokines and growth factors including IP-10, MIP-1β, MCP-1, IL-8, TNF-α and G-CSF. The released factors differed both in type and amount from those released by macrophages treated with the same viral protein. Moreover, Nef treatment slightly reduces the production of small EVs, and the protein was found associated with the small (size < 200 nm) but not the medium/large vesicles (size > 200 nm) collected from GEN2.2 cells. These results add new information on the interactions between this virulence factor and uninfected pDCs, and may provide the basis for further studies on the interactions of Nef protein with primary pDCs.

Spi-B is critical for plasmacytoid dendritic cell function and development

Blood ◽  
2012 ◽  
Vol 120 (24) ◽  
pp. 4733-4743 ◽  
Author(s):  
Izumi Sasaki ◽  
Katsuaki Hoshino ◽  
Takahiro Sugiyama ◽  
Chihiro Yamazaki ◽  
Takahiro Yano ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Dendritic Cell ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Plasmacytoid Dendritic Cell ◽  
Cell Subset ◽  
Type I ◽  
Dendritic Cell Subset ◽  
Type I Ifn ◽  
Deficient Mice

Abstract Plasmacytoid dendritic cells (pDCs), originating from hematopoietic progenitor cells in the BM, are a unique dendritic cell subset that can produce large amounts of type I IFNs by signaling through the nucleic acid–sensing TLR7 and TLR9 (TLR7/9). The molecular mechanisms for pDC function and development remain largely unknown. In the present study, we focused on an Ets family transcription factor, Spi-B, that is highly expressed in pDCs. Spi-B could transactivate the type I IFN promoters in synergy with IFN regulatory factor 7 (IRF-7), which is an essential transcription factor for TLR7/9-induced type I IFN production in pDCs. Spi-B–deficient pDCs and mice showed defects in TLR7/9-induced type I IFN production. Furthermore, in Spi-B–deficient mice, BM pDCs were decreased and showed attenuated expression of a set of pDC-specific genes whereas peripheral pDCs were increased; this uneven distribution was likely because of defective retainment of mature nondividing pDCs in the BM. The expression pattern of cell-surface molecules in Spi-B–deficient mice indicated the involvement of Spi-B in pDC development. The developmental defects of pDCs in Spi-B–deficient mice were more prominent in the BM than in the peripheral lymphoid organs and were intrinsic to pDCs. We conclude that Spi-B plays critical roles in pDC function and development.

A CD2 high‐expressing stress‐resistant human plasmacytoid dendritic‐cell subset

2016 ◽  
Vol 94 (5) ◽  
pp. 447-457 ◽  
Author(s):  
Christian Bryant ◽  
Phillip D Fromm ◽  
Fiona Kupresanin ◽  
Georgina Clark ◽  
Kenneth Lee ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Plasmacytoid Dendritic Cell ◽  
Cell Subset ◽  
Dendritic Cell Subset

scholarly journals The BXH2 mutation in IRF8 differentially impairs dendritic cell subset development in the mouse

Blood ◽  
2008 ◽  
Vol 111 (4) ◽  
pp. 1942-1945 ◽  
Author(s):  
Prafullakumar Tailor ◽  
Tomohiko Tamura ◽  
Herbert C. Morse ◽  
Keiko Ozato
Keyword(s):  
Dendritic Cell ◽  
Chromatin Immunoprecipitation ◽  
Cell Subset ◽  
Type I Interferons ◽  
Type I ◽  
Dendritic Cell Subset ◽  
Regulatory Factor ◽  
Mobility Shift ◽  
Type I Ifns ◽  
Plasmacytoid Dcs

Among dendritic cell (DC) subsets, CD8α+ DCs and plasmacytoid DCs (pDCs) produce high levels of IL12 and type I interferons (IFNs), respectively, and confer early innate immunity. Development of CD8α+ DCs and pDCs requires the interferon regulatory factor 8 (IRF8). Recently, a spontaneous point mutation was identified in the Irf8/Icsbp gene in the BXH2 mouse, which exhibits an immunodeficient phenotype similar to the IRF8 knockout (KO) mouse. We show that this mutation, designated IRF8R294C, abolishes the development of CD8α+ DCs without impairing pDC development, and eliminates production of IL12p40, while retaining that of type I IFNs. Electrophoretic mobility shift and chromatin immunoprecipitation assays indicated that IRF8R294C failed to interact with partner transcription factors and did not bind certain promoters that require partner interactions. Together, this work indicates that IRF8-partner interactions play different roles in CD8α+ DCs and pDCs, revealing a mechanistic separation that underlies development of these DC subsets.

scholarly journals Virus-induced Interferon α Production by a Dendritic Cell Subset in the Absence of Feedback Signaling In Vivo

2002 ◽  
Vol 195 (4) ◽  
pp. 507-516 ◽  
Author(s):  
Winfried Barchet ◽  
Marina Cella ◽  
Bernhard Odermatt ◽  
Carine Asselin-Paturel ◽  
Marco Colonna ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Marginal Zone ◽  
Viral Infections ◽  
Cell Subset ◽  
Interferon Α ◽  
Type I ◽  
Dendritic Cell Subset ◽  
Type I Ifn ◽  
High Level

An effective type I interferon (IFN-α/β) response is critical for the control of many viral infections. Here we show that in vesicular stomatitis virus (VSV)-infected mouse embryonic fibroblasts (MEFs) the production of IFN-α is dependent on type I IFN receptor (IFNAR) triggering, whereas in infected mice early IFN-α production is IFNAR independent. In VSV-infected mice type I IFN is produced by few cells located in the marginal zone of the spleen. Unlike other dendritic cell (DC) subsets, FACS®-sorted CD11cintCD11b−GR-1+ DCs show high IFN-α expression, irrespective of whether they were isolated from VSV-infected IFNAR-competent or -deficient mice. Thus, VSV preferentially activates a specialized DC subset presumably located in the marginal zone to produce high-level IFN-α largely independent of IFNAR feedback signaling.

scholarly journals IL-4 supports the generation of a dendritic cell subset from murine bone marrow with altered endocytosis capacity

2004 ◽  
Vol 77 (4) ◽  
pp. 535-543 ◽  
Author(s):  
Mauritius Menges ◽  
Thomas Baumeister ◽  
Susanne Rössner ◽  
Patrizia Stoitzner ◽  
Nikolaus Romani ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cell ◽  
Cell Subset ◽  
Dendritic Cell Subset ◽  
Murine Bone Marrow

scholarly journals Macrophage and dendritic cell subset composition can distinguish endotypes in adjuvant-induced asthma mouse models

2021 ◽  
Author(s):  
Müge Özkan ◽  
Yusuf Cem Eskiocak ◽  
Gerhard Wingender
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Mouse Models ◽  
Cell Subset ◽  
Clear Understanding ◽  
Dendritic Cell Subset ◽  
Myeloid Dendritic Cells ◽  
Differential Distribution ◽  
Eosinophilic Asthma ◽  
Effective Diagnosis

Asthma is a heterogeneous disease with neutrophilic and eosinophilic asthma as the main endotypes that are distinguished according to the cells recruited to the airways and the related pathology. Eosinophilic asthma is the treatment-responsive endotype, which is mainly associated with allergic asthma. Neutrophilic asthma is a treatment-resistant endotype, affecting 5-10% of asthmatics. Although eosinophilic asthma is well-studied, a clear understanding of the endotypes is essential to devise effective diagnosis and treatment approaches for neutrophilic asthma. To this end, we directly compared adjuvant-induced mouse models of neutrophilic (CFA/OVA) and eosinophilic (Alum/OVA) asthma side-by-side. The immune response in the inflamed lung was analyzed by multi-parametric flow cytometry and immunofluorescence. We found that eosinophilic asthma was characterized by a preferential recruitment of interstitial macrophages and myeloid dendritic cells, whereas in neutrophilic asthma plasmacytoid dendritic cells, exudate macrophages, and GL7 + activated B cells predominated. This differential distribution of macrophage and dendritic cell subsets reveals important aspects of the pathophysiology of asthma and holds the promise to be used as biomarkers to diagnose asthma endotypes.

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