scholarly journals Contribution of STAT1 to innate and adaptive immunity during type I interferon-mediated lethal virus infection

2020 ◽  
Vol 16 (4) ◽  
pp. e1008525 ◽  
Author(s):  
So Ri Jung ◽  
Thomas M. Ashhurst ◽  
Phillip K. West ◽  
Barney Viengkhou ◽  
Nicholas J. C. King ◽  
...  
Keyword(s):  
Virus Infection ◽  
Adaptive Immunity ◽  
Type I Interferon ◽  
Type I ◽  
Innate And Adaptive Immunity

scholarly journals CD40 Enhances Type I Interferon Responses Downstream of CD47 Blockade, Bridging Innate and Adaptive Immunity

2019 ◽  
Vol 8 (2) ◽  
pp. 230-245
Author(s):  
Suresh de Silva ◽  
George Fromm ◽  
Casey W. Shuptrine ◽  
Kellsey Johannes ◽  
Arpita Patel ◽  
...  
Keyword(s):  
Adaptive Immunity ◽  
Type I Interferon ◽  
Type I ◽  
Innate And Adaptive Immunity ◽  
Interferon Responses

Primary infection with simian immunodeficiency virus: plasmacytoid dendritic cell homing to lymph nodes, type I interferon, and immune suppression

Blood ◽  
2008 ◽  
Vol 112 (12) ◽  
pp. 4598-4608 ◽  
Author(s):  
Benoît Malleret ◽  
Benjamin Manéglier ◽  
Ingrid Karlsson ◽  
Pierre Lebon ◽  
Michelina Nascimbeni ◽  
...  
Keyword(s):  
T Cell ◽  
Lymph Nodes ◽  
Simian Immunodeficiency Virus ◽  
Adaptive Immunity ◽  
Immune Suppression ◽  
Primary Infection ◽  
Type I Interferon ◽  
Type I ◽  
Innate And Adaptive Immunity ◽  
Immunodeficiency Virus

AbstractPlasmacytoid dendritic cells (pDCs) are antigen-presenting cells that develop into type-I interferon (IFN-I)–producing cells in response to pathogens. Their role in human immunodeficiency virus (HIV) pathogenesis needs to be understood. We analyzed their dynamics in relation to innate and adaptive immunity very early during the acute phase of simian immunodeficiency virus (SIV) infection in 18 macaques. pDC counts decreased in blood and increased in peripheral lymph nodes, consistent with early recruitment in secondary lymphoid tissues. These changes correlated with the kinetic and intensity of viremia and were associated with a peak of plasma IFN-I. IFN-I and viremia were positively correlated with functional activity of the immune suppression associated enzyme indoleamine-2,3-dioxygenase (IDO) and FoxP3+CD8+ T cells, which both negatively correlated with SIV-specific T-cell proliferation and CD4+ T-cell activation. These data suggest that pDCs and IFN-I play a key role in shaping innate and adaptive immunity toward suppressive pathways during the acute phase of SIV/HIV primary infection.

scholarly journals The Efficacy of Radiotherapy Relies upon Induction of Type I Interferon–Dependent Innate and Adaptive Immunity

2011 ◽  
Vol 71 (7) ◽  
pp. 2488-2496 ◽  
Author(s):  
Byron C. Burnette ◽  
Hua Liang ◽  
Youjin Lee ◽  
Lukasz Chlewicki ◽  
Nikolai N. Khodarev ◽  
...  
Keyword(s):  
Adaptive Immunity ◽  
Type I Interferon ◽  
Type I ◽  
Innate And Adaptive Immunity

The Natural Alliance Between Type I Interferon and Dendritic Cells and Its Role in Linking Innate and Adaptive Immunity

2002 ◽  
Vol 22 (11) ◽  
pp. 1071-1080 ◽  
Author(s):  
Stefano M. Santini ◽  
Tiziana Di Pucchio ◽  
Caterina Lapenta ◽  
Stefania Parlato ◽  
Mariantonia Logozzi ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Adaptive Immunity ◽  
Type I Interferon ◽  
Type I ◽  
Innate And Adaptive Immunity

scholarly journals Mayaro virus replication restriction and induction of muscular inflammation in mice are dependent on age and type-I interferon response

2019 ◽  
Author(s):  
CM Figueiredo ◽  
RL Neris ◽  
DG Leopoldino ◽  
JS Almeida ◽  
JS dos-Santos ◽  
...  
Keyword(s):  
Adaptive Immunity ◽  
Type I Interferon ◽  
Interferon Response ◽  
Type I ◽  
Adult Type ◽  
Innate And Adaptive Immunity ◽  
High Prevalence ◽  
Interferon Receptor ◽  
Mayaro Virus ◽  
Deficient Mice

AbstractMayaro virus (MAYV) is an emergent Arbovirus belonging to the Alphavirus genus from theTogaviridaefamily which has been circulated in forest regions of American continent through small outbreaks. Recent studies warned for the risk of MAYV dispersion to new areas and for the potential establishment of an urban epidemic cycle. Similar to Chikungunya and other arthritogenic Alphavirus, MAYV-induced disease shows a high prevalence of arthralgia and myalgia that can persist for months. Despite this, knowledge regarding pathogenesis, characteristics of host immune response, and resolution of MAYV infections are still limited. Here we investigated the dependence of age, innate and adaptive immunity for the control of MAYV replication and induction of inflammation in mice. We observed that age and type I interferon response are related to restriction of MAYV infection and tissue inflammation in mice. Moreover, we showed that MAYV continues to replicate persistently in adult recombination activation gene-1 efficient mice (RAG1−/−), indicating that adaptive immunity is essential to MAYV clearance. Despite chronic replication, infected adult RAG1−/−mice did not develop an apparent signal of muscle damage at late infection. On the other hand, MAYV infection induces muscular and paw inflammation in young WT and adult Type I Interferon receptor deficient mice (IFNAR−/−). In addition, MAYV infection triggers an increase in the expression of pro-inflammatory mediators, such as TNF, IL-6, KC, IL-1β, MCP-1, and RANTES, in muscle tissue, and decreases TGF-β expression. Taken together, our study contributes to the comprehension of MAYV pathogenesis, and describes a translational mouse model for further studies of MAYV infection, as well for testing vaccine and therapeutic strategies against this virus.Author SummaryMAYV-induced disease presents a high prevalence of arthralgia and myalgia that potentially persist for months, which is characteristic of the arthritogenic Alphavirus group. However, information regarding MAYV infection and the molecular mechanism of pathogenesis is still scarce. Here we investigated the dependence of age, innate and adaptive immunity for the control of MAYV replication and induction of inflammation in mice. We observed that tissue inflammation and the restriction of MAYV replication in mice are affected by aging and type I interferon response. Besides, we also showed that adaptive immunity was important for MAYV clearance in adult mice. Histological analyses demonstrated that MAYV replication triggered muscular and paw inflammation in young WT and adult type-I interferon receptor deficient mice. In addition, the level of expression of several pro-inflammatory cytokines was increased in the muscle MAYV-infected mice. Our data provide an advance for understanding the molecular mechanism involved in MAYV pathogenesis, as well as describes anin vivomodel for further investigations on MAYV infection and for antiviral compounds and vaccine testing.

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