The Regulatory Role of Dendritic Cells in the Innate Immune Response

2014 ◽  
pp. 95-109 ◽  
Author(s):  
F. Granucci ◽  
S. Feau ◽  
I. Zanoni ◽  
G. Raimondi ◽  
N. Pavelka ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Regulatory Role

scholarly journals Role of Glycogen Synthase Kinase 3 (GSK-3) in innate immune response of human immature dendritic cells toAspergillus fumigatus

2010 ◽  
Vol 48 (4) ◽  
pp. 589-597 ◽  
Author(s):  
Katrin Spinnler ◽  
Markus Mezger ◽  
Michael Steffens ◽  
Helga Sennefelder ◽  
Oliver Kurzai ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Innate Immune Response ◽  
Glycogen Synthase ◽  
Innate Immune ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3 ◽  
Immature Dendritic Cells

scholarly journals Role of Dendritic Cells and Alveolar Macrophages in Regulating Early Host Defense against Pulmonary Infection with Cryptococcus neoformans

2009 ◽  
Vol 77 (9) ◽  
pp. 3749-3758 ◽  
Author(s):  
John J. Osterholzer ◽  
Jami E. Milam ◽  
Gwo-Hsiao Chen ◽  
Galen B. Toews ◽  
Gary B. Huffnagle ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Cryptococcus Neoformans ◽  
Innate Immune Response ◽  
Host Defense ◽  
Alveolar Macrophages ◽  
Pulmonary Infection ◽  
Innate Immune ◽  
Cellular Mechanisms

ABSTRACT Successful pulmonary clearance of the encapsulated yeast Cryptococcus neoformans requires a T1 adaptive immune response. This response takes up to 3 weeks to fully develop. The role of the initial, innate immune response against the organism is uncertain. In this study, an established model of diphtheria toxin-mediated depletion of resident pulmonary dendritic cells (DC) and alveolar macrophages (AM) was used to assess the contribution of these cells to the initial host response against cryptococcal infection. The results demonstrate that depletion of DC and AM one day prior to infection results in rapid clinical deterioration and death of mice within 6 days postinfection; this effect was not observed in infected groups of control mice not depleted of DC and AM. Depletion did not alter the microbial burden or total leukocyte recruitment in the lung. Mortality (in mice depleted of DC and AM) was associated with increased neutrophil and B-cell accumulation accompanied by histopathologic evidence of suppurative neutrophilic bronchopneumonia, cyst formation, and alveolar damage. Collectively, these data define an important role for DC and AM in regulating the initial innate immune response following pulmonary infection with C. neoformans. These findings provide important insight into the cellular mechanisms which coordinate early host defense against an invasive fungal pathogen in the lung.

scholarly journals The role of beneficial bacteria wall elasticity in regulating innate immune response

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Viktoria V. Мokrozub ◽  
Liudmyla M. Lazarenko ◽  
Liubov M. Sichel ◽  
Lidia P. Babenko ◽  
Petro M. Lytvyn ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Beneficial Bacteria

scholarly journals microRNA-210 and microRNA-3570 Negatively Regulate NF-κB-Mediated Inflammatory Responses by Targeting RIPK2 in Teleost Fish

2021 ◽  
Vol 12 ◽  
Author(s):  
Hui Su ◽  
Renjie Chang ◽  
Weiwei Zheng ◽  
Yuena Sun ◽  
Tianjun Xu
Keyword(s):  
Immune Response ◽  
Signaling Pathway ◽  
Innate Immune Response ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Regulatory Role ◽  
Inflammatory Cytokine Production ◽  
Immune Genes ◽  
Lower Vertebrates ◽  
Antimicrobial Immunity

Pathogen infection can cause the production of inflammatory cytokines, which are key mediators that cause the host’s innate immune response. Therefore, proper regulation of immune genes associated with inflammation is essential for immune response. Among them, microRNAs (miRNAs) as gene regulator have been widely reported to be involved in the innate immune response of mammals. However, the regulatory network in which miRNAs are involved in the development of inflammation is largely unknown in lower vertebrates. Here, we identified two miRNAs from miiuy croaker (Miichthys miiuy), miR-210 and miR-3570, which play a negative regulatory role in host antibacterial immunity. We found that the expressions of miR-210 and miR-3570 were significantly upregulated under the stimulation of Gram-negative bacterium vibrio harveyi and LPS (lipopolysaccharide). Induced miR-210 and miR-3570 inhibit inflammatory cytokine production by targeting RIPK2, thereby avoiding excessive inflammation. In particular, we found that miR-210 and miR-3570 negatively regulate antimicrobial immunity by regulating the RIPK2-mediated NF-κB signaling pathway. The collective results indicated that both miRNAs are used as negative feedback regulators to regulate RIPK2-mediated NF-κB signaling pathway and thus play a regulatory role in bacteria-induced inflammatory response.

scholarly journals Interferon-Stimulated Genes as Enhancers of Antiviral Innate Immune Signaling

2017 ◽  
Vol 10 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Keaton M. Crosse ◽  
Ebony A. Monson ◽  
Michael R. Beard ◽  
Karla J. Helbig
Keyword(s):  
Immune Response ◽  
Viral Infection ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Regulatory Factor ◽  
Interferon Stimulated Genes ◽  
Innate Immune Signaling ◽  
Recent Advancement ◽  
Antiviral Function

The ability of a host to curb a viral infection is heavily reliant on the effectiveness of an initial antiviral innate immune response, resulting in the upregulation of interferon (IFN) and, subsequently, IFN-stimulated genes (ISGs). ISGs serve to mount an antiviral state within a host cell, and although the specific antiviral function of a number of ISGs has been characterized, the function of many of these ISGs remains to be determined. Recent research has uncovered a novel role for a handful of ISGs, some of them directly induced by IFN regulatory factor 3 in the absence of IFN itself. These ISGs, most with potent antiviral activity, are also able to augment varying arms of the innate immune response to viral infection, thereby strengthening this response. This new understanding of the role of ISGs may, in turn, help the recent advancement of novel therapeutics aiming to augment innate signaling pathways in an attempt to control viral infection and pathogenesis.

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