scholarly journals Kinetics and expression patterns of chemokine receptors in human CD4+ T lymphocytes primed by myeloid or plasmacytoid dendritic cells

2003 ◽  
Vol 33 (2) ◽  
pp. 474-482 ◽  
Author(s):  
Anja Langenkamp ◽  
Kinya Nagata ◽  
Kristine Murphy ◽  
Lijun Wu ◽  
Antonio Lanzavecchia ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Lymphocytes ◽  
Chemokine Receptors ◽  
Expression Patterns ◽  
Plasmacytoid Dendritic Cells

DC-SIGN (dendritic cell-specific ICAM-grabbing non-integrin) and DC-SIGN-related (DC-SIGNR): friend or foe?

2003 ◽  
Vol 104 (4) ◽  
pp. 437-446 ◽  
Author(s):  
Elizabeth J. SOILLEUX
Keyword(s):  
Endothelial Cells ◽  
Dendritic Cells ◽  
Dendritic Cell ◽  
T Lymphocytes ◽  
High Efficiency ◽  
Immunoglobulin E ◽  
Expression Patterns ◽  
Intercellular Adhesion Molecule ◽  
Carbohydrate Binding ◽  
Wide Range

C-type lectins are calcium-dependent carbohydrate-binding proteins with a wide range of biological functions, many of which are related to immunity. DC-SIGN (dendritic cell-specific ICAM-grabbing non-integrin, where ICAM is intercellular adhesion molecule) is a recently described mannose-specific C-type lectin expressed by dendritic cells. Dendritic cells are potent antigen-presenting cells capable of activating T-lymphocytes. DC-SIGN, which is expressed by dendritic cells, binds to ICAM-3 on T-lymphocytes, therefore playing an important role in the activation of T-lymphocytes. DC-SIGN can also bind HIV, and the virus may remain bound to DC-SIGN for protracted periods. DC-SIGN may deliver bound HIV to permissive cell types, mediating infection with high efficiency. A closely related C-type lectin, DC-SIGN-related molecule (DC-SIGNR) has also been described. DC-SIGNR is expressed by restricted subsets of endothelial cells, but has similar ICAM-3 and HIV-binding properties to DC-SIGN. This review describes the mapping of DC-SIGN and DC-SIGNR to chromosome 19p13.3 adjacent to the previously described C-type lectin, CD23 [the low-affinity receptor for immunoglobulin E (FcERII)]. The similar genomic organization of these three genes is discussed and consideration is given to the evolutionary duplications that may underlie this arrangement. Both DC-SIGN and DC-SIGNR possess a neck region, made up of multiple repeats, which supports the ligand-binding domain. Consideration is given to the biological reasons underlying the considerable polymorphism in the numbers of repeats in DC-SIGNR, but not DC-SIGN. The expression patterns of both DC-SIGN and DC-SIGNR are discussed in detail, with particular attention to the expression of both molecules in the placenta, which may have implications for the vertical transmission of HIV. Since dendritic cells may be important in determining the phenotype of many immune responses, via effects on T-lymphocytes, the differential expression of DC-SIGN by particular dendritic cell subsets may have important implications for the immunobiological functions of DC-SIGN. Similarly, the expression of DC-SIGNR by very restricted subsets of endothelial cells may give clues to the function of DC-SIGNR. Finally, the role of DC-SIGN in pathology, particularly in infective and neoplastic processes, is discussed, followed by speculation about likely future developments in this field.

scholarly journals Activation and selective IL-17 response of human Vγ9Vδ2 T lymphocytes by TLR-activated plasmacytoid dendritic cells

Oncotarget ◽  
2016 ◽  
Vol 7 (38) ◽  
pp. 60896-60905 ◽  
Author(s):  
Elena Lo Presti ◽  
Nadia Caccamo ◽  
Valentina Orlando ◽  
Francesco Dieli ◽  
Serena Meraviglia
Keyword(s):  
Dendritic Cells ◽  
T Lymphocytes ◽  
Plasmacytoid Dendritic Cells

scholarly journals Broadly Neutralizing Antibody VRC01 Prevents HIV-1 Transmission from Plasmacytoid Dendritic Cells to CD4 T Lymphocytes

2014 ◽  
Vol 88 (18) ◽  
pp. 10975-10981 ◽  
Author(s):  
B. Su ◽  
A. Lederle ◽  
G. Laumond ◽  
C. Ducloy ◽  
S. Schmidt ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Lymphocytes ◽  
Neutralizing Antibody ◽  
Plasmacytoid Dendritic Cells ◽  
Broadly Neutralizing Antibody ◽  
Hiv 1

scholarly journals Cutting Edge: Selective Usage of Chemokine Receptors by Plasmacytoid Dendritic Cells

2001 ◽  
Vol 167 (4) ◽  
pp. 1862-1866 ◽  
Author(s):  
Giuseppe Penna ◽  
Silvano Sozzani ◽  
Luciano Adorini
Keyword(s):  
Dendritic Cells ◽  
Chemokine Receptors ◽  
Plasmacytoid Dendritic Cells ◽  
Cutting Edge

scholarly journals Bone Marrow Regulatory T Cells Are a Unique Population, Supported by Niche-Specific Cytokines and Plasmacytoid Dendritic Cells, and Required for Chronic Graft-Versus-Host Disease Control

2021 ◽  
Vol 9 ◽  
Author(s):  
Jemma Nicholls ◽  
Benjamin Cao ◽  
Laetitia Le Texier ◽  
Laura Yan Xiong ◽  
Christopher R. Hunter ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
T Cell ◽  
Graft Versus Host Disease ◽  
Chemokine Receptors ◽  
Cell Cycle Control ◽  
Plasmacytoid Dendritic Cells ◽  
Host Disease ◽  
Graft Versus Host

Regulatory T cell (Treg) reconstitution is essential for reestablishing tolerance and maintaining homeostasis following stem-cell transplantation. We previously reported that bone marrow (BM) is highly enriched in autophagy-dependent Treg and autophagy disruption leads to a significant Treg loss, particularly BM-Treg. To correct the known Treg deficiency observed in chronic graft-versus-host disease (cGVHD) patients, low dose IL-2 infusion has been administered, substantially increasing peripheral Treg (pTreg) numbers. However, as clinical responses were only seen in ∼50% of patients, we postulated that pTreg augmentation was more robust than for BM-Treg. We show that BM-Treg and pTreg have distinct characteristics, indicated by differential transcriptome expression for chemokine receptors, transcription factors, cell cycle control of replication and genes linked to Treg function. Further, BM-Treg were more quiescent, expressed lower FoxP3, were highly enriched for co-inhibitory markers and more profoundly depleted than splenic Treg in cGVHD mice. In vivo our data are consistent with the BM and not splenic microenvironment is, at least in part, driving this BM-Treg signature, as adoptively transferred splenic Treg that entered the BM niche acquired a BM-Treg phenotype. Analyses identified upregulated expression of IL-9R, IL-33R, and IL-7R in BM-Treg. Administration of the T cell produced cytokine IL-2 was required by splenic Treg expansion but had no impact on BM-Treg, whereas the converse was true for IL-9 administration. Plasmacytoid dendritic cells (pDCs) within the BM also may contribute to BM-Treg maintenance. Using pDC-specific BDCA2-DTR mice in which diptheria toxin administration results in global pDC depletion, we demonstrate that pDC depletion hampers BM, but not splenic, Treg homeostasis. Together, these data provide evidence that BM-Treg and splenic Treg are phenotypically and functionally distinct and influenced by niche-specific mediators that selectively support their respective Treg populations. The unique properties of BM-Treg should be considered for new therapies to reconstitute Treg and reestablish tolerance following SCT.

scholarly journals Transcription factor Runx2 controls the development and migration of plasmacytoid dendritic cells

2013 ◽  
Vol 210 (11) ◽  
pp. 2151-2159 ◽  
Author(s):  
Catherine M. Sawai ◽  
Vanja Sisirak ◽  
Hiyaa S. Ghosh ◽  
Esther Z. Hou ◽  
Michele Ceribelli ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Transcription Factor ◽  
Chemokine Receptors ◽  
Bone Development ◽  
System Development ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Differentiated Cells ◽  
Immune System Development ◽  
And Migration

Plasmacytoid dendritic cells (pDCs) rapidly produce type I interferon (IFN-I) in response to viruses and are essential for antiviral immune responses. Although related to classical DCs (cDCs) in their development and expression profile, pDCs possess many distinct features. Unlike cDCs, pDCs develop in the bone marrow (BM) and emerge into peripheral lymphoid organs and tissues as fully differentiated cells. We now report that pDCs specifically express Runx2, a Runt family transcription factor that is essential for bone development. pDCs in Runx2-deficient mice developed normally in the BM but were greatly reduced in the periphery. The defect was cell-intrinsic and was associated with the retention of mature Ly49Q+ pDCs in the BM. Runx2 was required for the expression of several pDC-enriched genes, including the chemokine receptors Ccr2 and Ccr5. Mature pDCs expressed high levels of Ccr5 at the cell surface, and Ccr5-deficient pDCs in a competitive setting were reduced in the periphery relative to the BM. Thus, Runx2 is required for the emergence of mature BM pDCs into the periphery, in a process that is partially dependent on Ccr5. These results establish Runx2 as a lineage-specific regulator of immune system development.

scholarly journals Heterogeneity of lung mononuclear phagocytes during pneumonia: contribution of chemokine receptors

2013 ◽  
Vol 305 (10) ◽  
pp. L702-L711 ◽  
Author(s):  
Lanlin Chen ◽  
Zhimin Zhang ◽  
Kathryn E. Barletta ◽  
Marie D. Burdick ◽  
Borna Mehrad
Keyword(s):  
Dendritic Cells ◽  
Alveolar Macrophages ◽  
Chemokine Receptors ◽  
Bacterial Pneumonia ◽  
Plasmacytoid Dendritic Cells ◽  
Mononuclear Phagocytes ◽  
Detectable Effect ◽  
Klebsiella Pneumonia ◽  
Blood Monocytes ◽  
Inflammatory Macrophages

Bacterial pneumonia is a common and dangerous illness. Mononuclear phagocytes, which comprise monocyte, resident and recruited macrophage, and dendritic cell subsets, are critical to antimicrobial defenses, but the dynamics of their recruitment to the lungs in pneumonia is not established. We hypothesized that chemokine-mediated traffic of mononuclear phagocytes is important in defense against bacterial pneumonia. In a mouse model of Klebsiella pneumonia, circulating Ly6Chiand, to a lesser extent, Ly6Clomonocytes expanded in parallel with accumulation of inflammatory macrophages and CD11bhidendritic cells and plasmacytoid dendritic cells in the lungs, whereas numbers of alveolar macrophages remained constant. CCR2 was expressed by Ly6Chimonocytes, recruited macrophages, and airway dendritic cells; CCR6 was prominently expressed by airway dendritic cells; and CX3CR1 was ubiquitously expressed by blood monocytes and lung CD11bhidendritic cells during infection. CCR2-deficient, but not CCL2-, CX3CR1-, or CCR6-deficient animals exhibited worse outcomes of infection. The absence of CCR2 had no detectable effect on neutrophils but resulted in reduction of all subsets of lung mononuclear phagocytes in the lungs, including alveolar macrophages and airway and plasmacytoid dendritic cells. In addition, absence of CCR2 skewed the phenotype of lung mononuclear phagocytes, abrogating the appearance of M1 macrophages and TNF-producing dendritic cells in the lungs. Taken together, these data define the dynamics of mononuclear phagocytes during pneumonia.

scholarly journals In situ leukemic plasmacytoid dendritic cells pattern of chemokine receptors expression and in vitro migratory response

Leukemia ◽  
2004 ◽  
Vol 18 (9) ◽  
pp. 1491-1498 ◽  
Author(s):  
N Bendriss-Vermare ◽  
L Chaperot ◽  
M Peoc'h ◽  
B Vanbervliet ◽  
M-C Jacob ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Chemokine Receptors ◽  
Plasmacytoid Dendritic Cells ◽  
Migratory Response
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