β-Defensins: Linking Innate and Adaptive Immunity Through Dendritic and T Cell CCR6

Science ◽  
1999 ◽  
Vol 286 (5439) ◽  
pp. 525-528 ◽  
Author(s):  
D. Yang ◽  
O. Chertov ◽  
S. N. Bykovskaia ◽  
Q. Chen ◽  
M. J. Buffo ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Cytoplasmic Membrane ◽  
Memory T Cells ◽  
Innate And Adaptive Immunity ◽  
Adaptive Immune ◽  
Microbial Invasion ◽  
Immature Dendritic Cells ◽  
Chemokine Ligand

Defensins contribute to host defense by disrupting the cytoplasmic membrane of microorganisms. This report shows that human β-defensins are also chemotactic for immature dendritic cells and memory T cells. Human β-defensin was selectively chemotactic for cells stably transfected to express human CCR6, a chemokine receptor preferentially expressed by immature dendritic cells and memory T cells. The β-defensin–induced chemotaxis was sensitive to pertussis toxin and inhibited by antibodies to CCR6. The binding of iodinated LARC, the chemokine ligand for CCR6, to CCR6-transfected cells was competitively displaced by β-defensin. Thus, β-defensins may promote adaptive immune responses by recruiting dendritic and T cells to the site of microbial invasion through interaction with CCR6.

scholarly journals Dendritic Cells under Hypoxia: How Oxygen Shortage Affects the Linkage between Innate and Adaptive Immunity

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Sandra Winning ◽  
Joachim Fandrey
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Adaptive Immune Response ◽  
Mature Dendritic Cell ◽  
Innate And Adaptive Immunity ◽  
Cell Functions ◽  
Adaptive Immune ◽  
Oxygen Shortage

Dendritic cells (DCs) are considered as one of the main regulators of immune responses. They collect antigens, process them, and present typical antigenic structures to lymphocytes, thereby inducing an adaptive immune response. All these processes take place under conditions of oxygen shortage (hypoxia) which is often not considered in experimental settings. This review highlights how deeply hypoxia modulates human as well as mouse immature and mature dendritic cell functions. It tries to linkin vitroresults to actualin vivostudies and outlines how hypoxia-mediated shaping of dendritic cells affects the activation of (innate) immunity.

Coexpression of αβ and γδ TCRs bridges innate and adaptive immunity

2020 ◽  
Vol 12 (546) ◽  
pp. eabc8941
Author(s):  
Gerald P. Morris
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Adaptive Immunity ◽  
Γδ T Cells ◽  
Adaptive Immune Responses ◽  
Innate And Adaptive Immunity ◽  
Adaptive Immune

T cells coexpressing αβ and γδ TCRs demonstrate characteristics of both αβ and γδ T cells, providing a link between innate and adaptive immune responses.

scholarly journals Dendritic Cells and Their Multiple Roles during Malaria Infection

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Kelly N. S. Amorim ◽  
Daniele C. G. Chagas ◽  
Fernando B. Sulczewski ◽  
Silvia B. Boscardin
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Antigen Presentation ◽  
Causative Agent ◽  
Malaria Infection ◽  
Multiple Roles ◽  
Key Factors ◽  
Adaptive Immune Responses ◽  
Adaptive Immune

Dendritic cells (DCs) play a central role in the initiation of adaptive immune responses, efficiently presenting antigens to T cells. This ability relies on the presence of numerous surface and intracellular receptors capable of sensing microbial components as well as inflammation and on a very efficient machinery for antigen presentation. In this way, DCs sense the presence of a myriad of pathogens, includingPlasmodiumspp., the causative agent of malaria. Despite many efforts to control this infection, malaria is still responsible for high rates of morbidity and mortality. Different groups have shown that DCs act duringPlasmodiuminfection, and data suggest that the phenotypically distinct DCs subsets are key factors in the regulation of immunity during infection. In this review, we will discuss the importance of DCs for the induction of immunity against the different stages ofPlasmodium, the outcomes of DCs activation, and also what is currently known aboutPlasmodiumcomponents that trigger such activation.

scholarly journals Gold nanoparticles (AuNPs) impair LPS-driven immune responses by promoting a tolerogenic-like dendritic cell phenotype with altered endosomal structures

Nanoscale ◽  
2021 ◽  
Author(s):  
Sara Michelini ◽  
Francesco Barbero ◽  
Alessandra Prinelli ◽  
Philip Steiner ◽  
Richard Weiss ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
T Cells ◽  
Dendritic Cells ◽  
Dendritic Cell ◽  
Immune Responses ◽  
Memory T Cells ◽  
Central Memory ◽  
Cell Phenotype ◽  
Th1 Cells ◽  
Central Memory T Cells

This study shows that gold nanoparticles promote the differentiation of dendritic cells to a tolerogenic-like phenotype, affecting their ability to induce antibacterial immune responses mediated by Th1 cells and to activate central memory T cells.

scholarly journals Regulation of Murine Dendritic Cell Immune Responses by Helicobacter felis Antigen

2006 ◽  
Vol 74 (8) ◽  
pp. 4624-4633 ◽  
Author(s):  
Maureen L. Drakes ◽  
Steven J. Czinn ◽  
Thomas G. Blanchard
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Dendritic Cell ◽  
Immune Responses ◽  
Lamina Propria ◽  
Adaptive Immune Responses ◽  
Helicobacter Felis ◽  
Adaptive Immune ◽  
Pulsed Dc ◽  
Antigen Presenting

ABSTRACT Helicobacter infections are present in approximately 50% of humans, causing severe illnesses such as gastritis and malignancies. Dendritic cells (DC) are critical antigen-presenting cells which link innate and adaptive immune responses. The mechanism of dendritic cell regulation in Helicobacter-induced gastritis is poorly understood. These studies characterized DC isolated from the lamina propria of Helicobacter-infected mice and analyzed innate and adaptive immune responses elicited by Helicobacter antigen (Ag)-pulsed DC. The presence of DC was elevated in the gastric lamina propria infiltrate of infected mice in comparison with controls. After treatment with Helicobacter felis Ag, DC were polarized to secrete interleukin-6 as the dominant cytokine. In the presence of DC and Helicobacter Ag, responder allogeneic T cells in culture exhibited limited cell division. We suggest that the response of DC and T cells to Helicobacter Ag is critical to the chronic persistence of Helicobacter-induced gastritis.

scholarly journals Antigen persistence and the control of local T cell memory by migrant respiratory dendritic cells after acute virus infection

2010 ◽  
Vol 207 (6) ◽  
pp. 1161-1172 ◽  
Author(s):  
Taeg S. Kim ◽  
Matthew M. Hufford ◽  
Jie Sun ◽  
Yang-Xin Fu ◽  
Thomas J. Braciale
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Virus Infection ◽  
Viral Antigen ◽  
Memory T Cells ◽  
Adaptive Immune ◽  
Virus Clearance ◽  
Antigen Persistence ◽  
The Impact

Acute viral infections induce robust adaptive immune responses resulting in virus clearance. Recent evidence suggests that there may be depots of viral antigen that persist in draining lymph nodes (DLNs) after virus clearance and could, therefore, affect the adaptive immune response and memory T cell formation. The nature of these residual antigen depots, the mechanism of antigen persistence, and the impact of the persistent antigen on memory T cells remain ill defined. Using a mouse model of influenza virus infection of the respiratory tract, we identified respiratory dendritic cells (RDCs) as essential for both sampling and presenting residual viral antigen. RDCs in the previously infected lung capture residual viral antigen deposited in an irradiation-resistant cell type. RDCs then transport the viral antigen to the LNs draining the site of infection, where they present the antigen to T cells. Lastly, we document preferential localization of memory T cells to the DLNs after virus clearance as a consequence of presentation of residual viral antigen by the migrant RDC.

The inhibitory receptor LILRB1 modulates the differentiation and regulatory potential of human dendritic cells

Blood ◽  
2008 ◽  
Vol 111 (6) ◽  
pp. 3090-3096 ◽  
Author(s):  
Neil T. Young ◽  
Edward C. P. Waller ◽  
Rashmi Patel ◽  
Ali Roghanian ◽  
Jonathan M. Austyn ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Inhibitory Receptor ◽  
Innate And Adaptive Immunity ◽  
Memory T Cell ◽  
Cell Responses ◽  
Adaptive Immune ◽  
Regulatory Potential ◽  
Human Dendritic Cells ◽  
Hla Molecules

Abstract Dendritic cells (DCs) link innate and adaptive immunity, initiating and regulating effector cell responses. They ubiquitously express members of the LILR (ILT, LIR, CD85) family of molecules, some of which recognize self-HLA molecules, but little is known of their possible functions in DC biology. We demonstrate that the inhibitory receptor LILRB1 (ILT2, LIR1, CD85j) is selectively up-regulated during DC differentiation from monocyte precursors in culture. Continuous ligation of LILRB1 modulated cellular differentiation, conferred a unique phenotype upon the resultant cells, induced a profound resistance to CD95-mediated cell death, and inhibited secretion of cytokines IL-10, IL-12p70, and TGF-β. These features remained stable even after exposure of the cells to bacterial LPS. Ligated DCs exhibited poor stimulatory activity for primary and memory T-cell proliferative responses, but this was substantially reversed by blockade of CD80 or its preferred ligand CTLA-4, or by depleting CD4+ CD25+ CD127lo regulatory T cells. Our findings suggest that ligation of LILRB1 on DCs by self-HLA molecules may play a key role in controlling the balance between the induction and suppression of adaptive immune responses.

Interleukin-17A modulates human airway epithelial responses to human rhinovirus infection

2007 ◽  
Vol 293 (2) ◽  
pp. L505-L515 ◽  
Author(s):  
Shahina Wiehler ◽  
David Proud
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Memory T Cells ◽  
Neutrophil Infiltration ◽  
Human Rhinovirus ◽  
Chronic Obstructive ◽  
Airway Epithelial ◽  
Activated T Cells ◽  
Obstructive Pulmonary Disease ◽  
Immature Dendritic Cells

Human rhinovirus (HRV) infections are associated with exacerbations of asthma and chronic obstructive pulmonary disease that are characterized by a selective neutrophil infiltration. IL-17A, a cytokine derived primarily from activated T cells, has been linked to neutrophilic inflammation of the airways. We hypothesized that IL-17A alters the response of HRV-infected epithelial cells to modulate airway inflammatory cell populations. IL-17A synergistically enhanced HRV-16-induced epithelial production of the neutrophil chemoattractant, IL-8, as well as human β-defensin-2 (HBD-2), a chemoattractant for immature dendritic cells and memory T cells, but suppressed viral production of the eosinophil chemoattractant, RANTES. These effects were not due to alterations of viral uptake or replication by IL-17A. The synergy between HRV-16 and IL-17A for IL-8 protein production was both dose- and time-dependent. IL-8 induction by IL-17A or HRV-16, alone and in combination, was reduced by inhibitors of the p38 and p44/42 MAPK pathways. By contrast, induction of HBD-2 depended on the activation of the p38 and JNK pathways. The ability of IL-17A to synergistically enhance HRV-induced IL-8 is mediated posttranscriptionally, since IL-8 promoter activation by the combination of the two stimuli was merely additive, whereas the combination of IL-17A and HRV-16 led to stabilization of IL-8 mRNA. Similarly, stimulation of HBD-2 promoter constructs by the combination of IL-17A and HRV-16 was no more than the sum of the individual responses. Further studies are needed to examine HBD-2 mRNA stability. Taken together, these data represent the first demonstration that IL-17A can modify epithelial responses to HRV in a manner that would be expected to favor the recruitment of neutrophils, immature dendritic cells, and memory T cells to the airways.

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