scholarly journals IL-15 Is Expressed by Dendritic Cells in Response to Type I IFN, Double-Stranded RNA, or Lipopolysaccharide and Promotes Dendritic Cell Activation

2001 ◽  
Vol 167 (3) ◽  
pp. 1179-1187 ◽  
Author(s):  
Fabrizio Mattei ◽  
Giovanna Schiavoni ◽  
Filippo Belardelli ◽  
David F. Tough
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Cell Activation ◽  
Type I ◽  
Type I Ifn ◽  
Dendritic Cell Activation ◽  
Double Stranded Rna

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 Rabies Virus Infection Induces Type I Interferon Production in an IPS-1 Dependent Manner While Dendritic Cell Activation Relies on IFNAR Signaling

2010 ◽  
Vol 6 (7) ◽  
pp. e1001016 ◽  
Author(s):  
Elizabeth J. Faul ◽  
Celestine N. Wanjalla ◽  
Mehul S. Suthar ◽  
Michael Gale ◽  
Christoph Wirblich ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Virus Infection ◽  
Rabies Virus ◽  
Cell Activation ◽  
Type I Interferon ◽  
Type I ◽  
Dependent Manner ◽  
Interferon Production ◽  
Dendritic Cell Activation ◽  
Rabies Virus Infection

scholarly journals A distinct subset of plasmacytoid dendritic cells induces activation and differentiation of B and T lymphocytes

2017 ◽  
Vol 114 (8) ◽  
pp. 1988-1993 ◽  
Author(s):  
Hong Zhang ◽  
Josh D. Gregorio ◽  
Toru Iwahori ◽  
Xiangyue Zhang ◽  
Okmi Choi ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Cell Activation ◽  
Plasmacytoid Dendritic Cells ◽  
T Cell Proliferation ◽  
Type I ◽  
Type I Ifn ◽  
Immune Functions ◽  
B Cell Activation ◽  
Cpg Oligonucleotides ◽  
B And T Lymphocytes

Plasmacytoid dendritic cells (pDCs) are known mainly for their secretion of type I IFN upon viral encounter. We describe a CD2hiCD5+CD81+pDC subset, distinguished by prominent dendrites and a mature phenotype, in human blood, bone marrow, and tonsil, which can be generated from CD34+progenitors. These CD2hiCD5+CD81+cells express classical pDC markers, as well as the toll-like receptors that enable conventional pDCs to respond to viral infection. However, their gene expression profile is distinct, and they produce little or no type I IFN upon stimulation with CpG oligonucleotides, likely due to their diminished expression of IFN regulatory factor 7. A similar population of CD5+CD81+pDCs is present in mice and also does not produce type I IFN after CpG stimulation. In contrast to conventional CD5−CD81−pDCs, human CD5+CD81+pDCs are potent stimulators of B-cell activation and antibody production and strong inducers of T-cell proliferation and Treg formation. These findings reveal the presence of a discrete pDC population that does not produce type I IFN and yet mediates important immune functions previously attributed to all pDCs.

scholarly journals Effects of Fatty Acid Oxidation and Its Regulation on Dendritic Cell-Mediated Immune Responses in Allergies: An Immunometabolism Perspective

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Shanfeng Sun ◽  
Yanjun Gu ◽  
Junjuan Wang ◽  
Cheng Chen ◽  
Shiwen Han ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Fatty Acid ◽  
Dendritic Cell ◽  
Immune Responses ◽  
Fatty Acid Oxidation ◽  
Cell Activation ◽  
Metabolic Reprogramming ◽  
Acid Oxidation ◽  
Dendritic Cell Activation ◽  
Functional Changes

Type 1 allergies, involve a complex interaction between dendritic cells and other immune cells, are pathological type 2 inflammatory immune responses against harmless allergens. Activated dendritic cells undergo extensive phenotypic and functional changes to exert their functions. The activation, differentiation, proliferation, migration, and mounting of effector reactions require metabolic reprogramming. Dendritic cells are important upstream mediators of allergic responses and are therefore an important effector of allergies. Hence, a better understanding of the underlying metabolic mechanisms of functional changes that promote allergic responses of dendritic cells could improve the prevention and treatment of allergies. Metabolic changes related to dendritic cell activation have been extensively studied. This review briefly outlines the basis of fatty acid oxidation and its association with dendritic cell immune responses. The relationship between immune metabolism and effector function of dendritic cells related to allergic diseases can better explain the induction and maintenance of allergic responses. Further investigations are warranted to improve our understanding of disease pathology and enable new treatment strategies.

scholarly journals Dendritic cells activated by double-stranded RNA induce arthritis via autocrine type I IFN signaling

2013 ◽  
Vol 95 (4) ◽  
pp. 661-666 ◽  
Author(s):  
S. C. Narendra ◽  
J. P. Chalise ◽  
N. Hook ◽  
M. Magnusson
Keyword(s):  
Dendritic Cells ◽  
Type I ◽  
Type I Ifn ◽  
Double Stranded Rna ◽  
Induce Arthritis

CD2 engagement induces dendritic cell activation: implications for immune surveillance and T-cell activation

Blood ◽  
2003 ◽  
Vol 102 (5) ◽  
pp. 1745-1752 ◽  
Author(s):  
Keith Crawford ◽  
Aleksandra Stark ◽  
Betsy Kitchens ◽  
Kerry Sternheim ◽  
Vassilios Pantazopoulos ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Dendritic Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Immune Surveillance ◽  
T Cell Proliferation ◽  
Dendritic Cell Activation ◽  
Adaptive Immune

Abstract We have shown previously that primary dendritic cells and monocytes express equal levels of CD14 but are distinguishable by the presence of CD2 on dendritic cells. CD2 is known to mediate the activation of T and natural killer (NK) cells through its interaction with CD58. CD2 epitopes recognized by anti-T111, -T112, and -T113 monoclonal antibodies (mAbs) are present on dendritic cells. Here we show that CD2 engagement significantly increases class II, costimulatory (CD40, CD80, CD86), adhesion (CD54, CD58), and CCR7 molecule expression on primary dendritic cells. Conversely, minimal or no change in the expression of the above antigens occurs on monocyte-derived dendritic cells, because these molecules are already maximally expressed. However, both kinds of dendritic cells release interleukin-1β (IL-1β) and IL-12 after CD2 engagement. Lastly, interference with dendritic cell CD2–T-cell CD58 engagement decreases naive CD4+CD45RA+ T-cell proliferation. Collectively, our results suggest another role of the CD2-CD58 pathway that allows nonimmune and immune cells to interact directly with dendritic cells and initiate innate and adaptive immune responses.

scholarly journals Selective control of type I IFN induction by the Rac activator DOCK2 during TLR-mediated plasmacytoid dendritic cell activation

2010 ◽  
Vol 207 (4) ◽  
pp. 721-730 ◽  
Author(s):  
Kazuhito Gotoh ◽  
Yoshihiko Tanaka ◽  
Akihiko Nishikimi ◽  
Risa Nakamura ◽  
Hisakata Yamada ◽  
...  
Keyword(s):  
Autoimmune Diseases ◽  
Signaling Pathway ◽  
Cell Activation ◽  
Nuclear Translocation ◽  
Plasmacytoid Dendritic Cell ◽  
Dominant Negative ◽  
Type I ◽  
Type I Ifn ◽  
Dendritic Cell Activation ◽  
Iκb Kinase

Plasmacytoid dendritic cells (pDCs) play a key role in antiviral immunity, but also contribute to the pathogenesis of certain autoimmune diseases, by producing large amounts of type I IFNs. Although activation of pDCs is triggered by engagement of nucleotide-sensing toll-like receptors (TLR) 7 and 9, type I IFN induction additionally requires IκB kinase (IKK) α–dependent activation of IFN regulatory factor (IRF) 7. However, the signaling pathway mediating IKK-α activation is poorly defined. We show that DOCK2, an atypical Rac activator, is essential for TLR7- and TLR9-mediated IFN-α induction in pDCs. We found that the exposure of pDCs to nucleic acid ligands induces Rac activation through a TLR-independent and DOCK2-dependent mechanism. Although this Rac activation was dispensable for induction of inflammatory cytokines, phosphorylation of IKK-α and nuclear translocation of IRF-7 were impaired in Dock2-deficient pDCs, resulting in selective loss of IFN-α induction. Similar results were obtained when a dominant-negative Rac mutant was expressed in wild-type pDCs. Thus, the DOCK2–Rac signaling pathway acts in parallel with TLR engagement to control IKK-α activation for type I IFN induction. Owing to its hematopoietic cell-specific expression, DOCK2 may serve as a therapeutic target for type I IFN–related autoimmune diseases.

scholarly journals A type I IFN–Flt3 ligand axis augments plasmacytoid dendritic cell development from common lymphoid progenitors

2013 ◽  
Vol 210 (12) ◽  
pp. 2515-2522 ◽  
Author(s):  
Yi-Ling Chen ◽  
Ting-Ting Chen ◽  
Li-Mei Pai ◽  
Joanna Wesoly ◽  
Hans A.R. Bluyssen ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cell ◽  
Critical Role ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Type I Ifn ◽  
Flt3 Ligand ◽  
Lymphoid Progenitors

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.

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