scholarly journals Type I and type III interferon-induced immune response: It's a matter of kinetics and magnitude

Hepatology ◽  
2014 ◽  
Vol 59 (4) ◽  
pp. 1225-1228 ◽  
Author(s):  
David Olagnier ◽  
John Hiscott
Keyword(s):  
Immune Response ◽  
Type I ◽  
Type Iii ◽  
Type Iii Interferon

scholarly journals Differential Regulation of Type I and Type III Interferon Signaling

2019 ◽  
Vol 20 (6) ◽  
pp. 1445 ◽  
Author(s):  
Megan L. Stanifer ◽  
Kalliopi Pervolaraki ◽  
Steeve Boulant
Keyword(s):  
Immune Response ◽  
Differential Regulation ◽  
Type I ◽  
Type Ii ◽  
Interferon Signaling ◽  
Type Iii ◽  
Type I Ifns ◽  
Current State ◽  
Type Iii Ifn ◽  
Type Iii Interferon

Interferons (IFNs) are very powerful cytokines, which play a key role in combatting pathogen infections by controlling inflammation and immune response by directly inducing anti-pathogen molecular countermeasures. There are three classes of IFNs: type I, type II and type III. While type II IFN is specific for immune cells, type I and III IFNs are expressed by both immune and tissue specific cells. Unlike type I IFNs, type III IFNs have a unique tropism where their signaling and functions are mostly restricted to epithelial cells. As such, this class of IFN has recently emerged as a key player in mucosal immunity. Since the discovery of type III IFNs, the last 15 years of research in the IFN field has focused on understanding whether the induction, the signaling and the function of these powerful cytokines are regulated differently compared to type I IFN-mediated immune response. This review will cover the current state of the knowledge of the similarities and differences in the signaling pathways emanating from type I and type III IFN stimulation.

Type-III interferon, not type-I, is the predominant interferon induced by respiratory viruses in nasal epithelial cells

2011 ◽  
Vol 160 (1-2) ◽  
pp. 360-366 ◽  
Author(s):  
Tamaki Okabayashi ◽  
Takashi Kojima ◽  
Tomoyuki Masaki ◽  
Shin-ichi Yokota ◽  
Tadaatsu Imaizumi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Respiratory Viruses ◽  
Type I ◽  
Nasal Epithelial Cells ◽  
Type Iii ◽  
Type Iii Interferon

scholarly journals Limited In Vivo Production of Type I or Type III Interferon After Infection of Macaques with Vaccine or Wild-Type Strains of Measles Virus

2015 ◽  
Vol 35 (4) ◽  
pp. 292-301 ◽  
Author(s):  
Rupak Shivakoti ◽  
Debra Hauer ◽  
Robert J. Adams ◽  
Wen-Hsuan W. Lin ◽  
William Paul Duprex ◽  
...  
Keyword(s):  
Measles Virus ◽  
Type I ◽  
Wild Type ◽  
Type Iii ◽  
Type Iii Interferon ◽  
Type Strains

PS1-53 Analysis of Type I and Type III interferon in sera from autoimmune diseases

Cytokine ◽  
2010 ◽  
Vol 52 (1-2) ◽  
pp. 28
Author(s):  
Thomas B. Lavoie ◽  
Yognandan Pandya ◽  
Michael Skawinski ◽  
Sara Crisafulli Cabatu ◽  
Jessica Esposito ◽  
...  
Keyword(s):  
Autoimmune Diseases ◽  
Type I ◽  
Type Iii ◽  
Type Iii Interferon

scholarly journals Critical role of type III interferon in controlling SARS-CoV-2 infection, replication and spread in primary human intestinal epithelial cells

2020 ◽  
Author(s):  
Megan L. Stanifer ◽  
Carmon Kee ◽  
Mirko Cortese ◽  
Sergio Triana ◽  
Markus Mukenhirn ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
De Novo ◽  
Intestinal Epithelial Cells ◽  
Critical Role ◽  
Type I ◽  
Intestinal Epithelial ◽  
Virus Particles ◽  
Type Iii ◽  
Human Intestinal Epithelial Cells ◽  
Type Iii Interferon

SummarySARS-CoV-2 is an unprecedented worldwide health problem that requires concerted and global approaches to better understand the virus in order to develop novel therapeutic approaches to stop the COVID-19 pandemic and to better prepare against potential future emergence of novel pandemic viruses. Although SARS-CoV-2 primarily targets cells of the lung epithelium causing respiratory infection and pathologies, there is growing evidence that the intestinal epithelium is also infected. However, the importance of the enteric phase of SARS-CoV-2 for virus-induced pathologies, spreading and prognosis remains unknown. Here, using both colon-derived cell lines and primary non-transformed colon organoids, we engage in the first comprehensive analysis of SARS-CoV-2 lifecycle in human intestinal epithelial cells. Our results demonstrate that human intestinal epithelial cells fully support SARS-CoV-2 infection, replication and production of infectious de-novo virus particles. Importantly, we identified intestinal epithelial cells as the best culture model to propagate SARS-CoV-2. We found that viral infection elicited an extremely robust intrinsic immune response where, interestingly, type III interferon mediated response was significantly more efficient at controlling SARS-CoV-2 replication and spread compared to type I interferon. Taken together, our data demonstrate that human intestinal epithelial cells are a productive site of SARS-CoV-2 replication and suggest that the enteric phase of SARS-CoV-2 may participate in the pathologies observed in COVID-19 patients by contributing in increasing patient viremia and by fueling an exacerbated cytokine response.

scholarly journals Type I and type III interferon in opposition?

2020 ◽  
Vol 20 (7) ◽  
pp. 406-406 ◽  
Author(s):  
Matthew D. Park
Keyword(s):  
Type I ◽  
Type Iii ◽  
Type Iii Interferon

TLR 7/8 regulates Type I and Type III Interferon Signalling in RV1b induced Allergic Asthma

2020 ◽  
pp. 2001562
Author(s):  
Jasmin Krug ◽  
Alexander Kiefer ◽  
Julia Koelle ◽  
Tytti Vuorinen ◽  
Paraskevi Xepapadaki ◽  
...  
Keyword(s):  
Preschool Age ◽  
Lung Cells ◽  
Type I ◽  
Mrna Levels ◽  
Toll Like Receptor ◽  
Type Iii ◽  
Β Receptor ◽  
Primary School Age ◽  
Interferon Responses ◽  
Type Iii Interferon

QuestionInterferon responses have been reported to be defective in rhinovirus (RV) induced asthma. The heterodimeric receptor of type I Interferon (IFN) (IFN-α/-β) is composed by IFNαR-1 and IFNαR-2. Ligand binding to the IFN-α/-β receptor complex activates STAT1 and STAT2 intracellularly. Although type III Interferon (IFN-λ) binds to a different receptor containing IFNλRA and IL-10R2, its triggering leads to activation of the same downstream transcription factors. Here we analysed the effects of Rhinovirus to Interferon type I and III receptors and asked about possible Toll-like receptor 7/8 agonist R848 mediated IFNαR1 and IFNλRα regulation.MethodsWe measured IFN-α, -β, -λ and their receptor levels in PBMCs supernatants and cell pellets stimulated with RV1b and the Toll-like Receptor 7/8 (TLR7/8) agonist (R848), in two cohorts of children with and without asthma recruited at preschool age (PreDicta) and at primary school age (AGENDAS) as well as in cell supernatants from total lung cells isolated from mice.ResultsWe observed that R848 induced IFNλR mRNA expression in PBMCs of healthy and asthmatic children, but suppressed the IFNαR mRNA levels. In murine lung cells, RV1balone and together with R848 suppressed IFNαR protein in T cells compared to controls and in total lung IFNλR mRNA compared to RV1b infection alone.AnswerIn PBMCs from pre-school children, IFNαR mRNA was reduced and IFNλRα mRNA was induced upon treatment with TLR7/8 agonist thus suggesting new avenues for induction of anti-viral immune responses in pediatric asthma.

scholarly journals Biological Effects of Chicken Type III Interferon on Expression of Interferon-Stimulated Genes in Chickens: Comparison with Type I and Type II Interferons

2012 ◽  
Vol 74 (11) ◽  
pp. 1381-1386 ◽  
Author(s):  
Yasumitsu MASUDA ◽  
Akiko MATSUDA ◽  
Tatsufumi USUI ◽  
Toru SUGAI ◽  
Atsushi ASANO ◽  
...  
Keyword(s):  
Biological Effects ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Interferon Stimulated Genes ◽  
Type Iii Interferon
Sign in / Sign up

Export Citation Format

Share Document