scholarly journals Symmetric Arginine Dimethylation Is Selectively Required for mRNA Splicing and the Initiation of Type I and Type III Interferon Signaling

Cell Reports ◽  
2020 ◽  
Vol 30 (6) ◽  
pp. 1935-1950.e8 ◽  
Author(s):  
Patrick J. Metz ◽  
Keith A. Ching ◽  
Tao Xie ◽  
Paulina Delgado Cuenca ◽  
Sherry Niessen ◽  
...  
Keyword(s):  
Mrna Splicing ◽  
Type I ◽  
Interferon Signaling ◽  
Type Iii ◽  
Type Iii Interferon

Distinct Roles of Type I and Type III Interferons During a Native Murine β Coronavirus Lung Infection

2021 ◽  
Author(s):  
Lokesh Sharma ◽  
Xiaohua Peng ◽  
Hua Qing ◽  
Brandon K. Hilliard ◽  
Jooyoung Kim ◽  
...  
Keyword(s):  
Type I Interferon ◽  
Lung Infection ◽  
Viral Clearance ◽  
Type I Interferons ◽  
Type I ◽  
Interferon Signaling ◽  
Type Iii ◽  
Coronavirus Infection ◽  
Type Iii Interferon

Coronaviruses are a major healthcare threat to humankind. Currently, the host factors that contribute to limit disease severity in healthy young patients are not well defined. Interferons are key antiviral molecules, especially type I and type III interferons. The role of these interferons during coronavirus disease is a subject of debate. Here using mice that are deficient in type I (IFNAR1 -/- ), type III (IFNLR1 -/- ) or both (IFNAR1/LR1 -/- ) interferon signaling pathways and murine adapted coronavirus (MHV-A59) administered through intranasal route, we define the role of interferons in coronavirus infection. We show that type I interferons play a major role in host survival in this model while a minimal role of type III interferons was manifested only in the absence of type I interferons or during a lethal dose of coronavirus. IFNAR1 -/- and IFNAR1/LR1 -/- mice had an uncontrolled viral burden in the airways and lung and increased viral dissemination to other organs. The absence of only type III interferon signaling had no measurable difference in the viral load. The increased viral load in IFNAR1 -/- and IFNAR1/LR1 -/- mice was associated with increased tissue injury, especially evident in the lung and liver. Type I but not type III interferon treatment was able to promote survival if treated during early disease. Further, we show that type I interferon signaling in macrophages contributes to the beneficial effects during coronavirus infection in mice. Importance: The antiviral and pathological potential of type I and type III interferons during coronavirus infection remains poorly defined and opposite findings have been reported. We report that both type I and type III interferons have anti-coronaviral activities, but their potency and organ specificity differ. Type I interferons deficiency rendered the mice susceptible to even a sublethal murine coronavirus infection, while the type III interferon deficiency impaired survival only during a lethal infection or during a sublethal infection in absence of type I interferon signaling. While treatment with both type I and III interferons promoted viral clearance in the airways and lung, only type I interferons promoted the viral clearance in the liver and improved host survival upon early treatment (12 hours post infection). This study demonstrates distinct roles and potency of type I and type III interferons and their therapeutic potential during coronavirus lung infection.

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.

scholarly journals Interferon Lambda Regulates Cellular and Humoral Immunity in Pristane-Induced Lupus

2021 ◽  
Vol 22 (21) ◽  
pp. 11747
Author(s):  
Tom Aschman ◽  
Sandra Schaffer ◽  
Stylianos Iason Biniaris Georgallis ◽  
Antigoni Triantafyllopoulou ◽  
Peter Staeheli ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Survival Rates ◽  
Mononuclear Phagocytes ◽  
Type I Interferons ◽  
Type I ◽  
Interferon Signaling ◽  
Type Iii ◽  
Cellular And Humoral Immunity ◽  
Type Iii Interferon

A pivotal role of type I interferons in systemic lupus erythematosus (SLE) is widely accepted. Type III interferons (IFN-λ) however, the most recently discovered cytokines grouped within the interferon family, have not been extensively studied in lupus disease models yet. Growing evidence suggests a role for IFN-λ in regulating both innate and adaptive immune responses, and increased serum concentrations have been described in multiple autoimmune diseases including SLE. Using the pristane-induced lupus model, we found that mice with defective IFN-λ receptors (Ifnlr1−/−) showed increased survival rates, decreased lipogranuloma formation and reduced anti-dsDNA autoantibody titers in the early phase of autoimmunity development compared to pristane-treated wild-type mice. Moreover, Ifnlr1−/− mice treated with pristane had reduced numbers of inflammatory mononuclear phagocytes and cNK cells in their kidneys, resembling untreated control mice. Systemically, circulating B cells and monocytes (CD115+Ly6C+) were reduced in pristane-treated Ifnlr1−/− mice. The present study supports a significant role for type III interferons in the pathogenesis of pristane-induced murine autoimmunity as well as in systemic and renal inflammation. Although the absence of type III interferon receptors does not completely prevent the development of autoantibodies, type III interferon signaling accelerates the development of autoimmunity and promotes a pro-inflammatory environment in autoimmune-prone hosts.

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

Regeneration After Radiation- and Immune-Mediated Tissue Injury Is Not Enhanced by Type III Interferon Signaling

2019 ◽  
Vol 103 (4) ◽  
pp. 970-976 ◽  
Author(s):  
Julius C. Fischer ◽  
Chia-Ching Lin ◽  
Simon Heidegger ◽  
Alexander Wintges ◽  
Martin Schlapschy ◽  
...  
Keyword(s):  
Tissue Injury ◽  
Interferon Signaling ◽  
Type Iii ◽  
Immune Mediated ◽  
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
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