1. |
|
|
2. |
|
|
3. |
|
|
4. |
|
|
5. |
|
|
6. |
- Christoffersson, G, et al.
(författare)
-
Mouse Models of Virus-Induced Type 1 Diabetes
- 2020
-
Ingår i: Methods in molecular biology (Clifton, N.J.). - New York, NY : Springer US. - 1940-6029. ; 2128, s. 93-105
-
Tidskriftsartikel (refereegranskat)
|
|
7. |
|
|
8. |
- Stone, Virginia M., et al.
(författare)
-
Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells-A Strategy Used by Coxsackie B Virus to Evade the Host's Innate Immune Response at the Primary Site of Infection?
- 2021
-
Ingår i: Microorganisms. - : MDPI AG. - 2076-2607. ; 9:1
-
Tidskriftsartikel (refereegranskat)abstract
- Increasing evidence highlights the importance of the antiviral activities of the type III interferons (IFN lambda s; IL-28A, IL-28B, IL29, and IFN lambda 4) in the intestine. However, many viruses have developed strategies to counteract these defense mechanisms by preventing the production of IFNs. Here we use infection models, a clinical virus isolate, and several molecular biology techniques to demonstrate that both type I and III IFNs induce an antiviral state and attenuate Coxsackievirus group B (CVB) replication in human intestinal epithelial cells (IECs). While treatment of IECs with a viral mimic (poly (I:C)) induced a robust expression of both type I and III IFNs, no such up-regulation was observed after CVB infection. The blunted IFN response was paralleled by a reduction in the abundance of proteins involved in the induction of interferon gene transcription, including TIR-domain-containing adapter-inducing interferon-beta (TRIF), mitochondrial antiviral-signaling protein (MAVS), and the global protein translation initiator eukaryotic translation initiation factor 4G (eIF4G). Taken together, this study highlights a potent anti-Coxsackieviral effect of both type I and III IFNs in cells located at the primary site of infection. Furthermore, we show for the first time that the production of type I and III IFNs in IECs is blocked by CVBs. These findings suggest that CVBs evade the host immune response in order to successfully infect the intestine.
|
|