What is interferon immunity?

Interferons are proteins that are part of your natural defenses. They tell your immune system that germs or cancer cells are in your body. And they trigger killer immune cells to fight those invaders. Interferons got their name because they “interfere” with viruses and keep them from multiplying.

What does interferon do to viruses?

Interferon is secreted by cells in response to stimulation by a virus or other foreign substance, but it does not directly inhibit the virus’s multiplication. Rather, it stimulates the infected cells and those nearby to produce proteins that prevent the virus from replicating within them.

What does IRF3 stand for?

IFN regulatory factor 3 (IRF3) is a transcription regulator of cellular responses in many cell types that is known to be essential for innate immunity.

What is the correct Iupac name for IRF3?

View/Edit Mouse. Interferon regulatory factor 3, also known as IRF3, is an interferon regulatory factor.

Who makes interferon?

Two drug companies manufacture pegylated interferon. Roche Products Ltd make Pegasys (interferon alpha 2A) and MSD make PegIntron (interferon alpha 2B).

Is the upregulation of interferon dependent on IRF3 expression?

Interferon-Independent Upregulation of Interferon-Stimulated Genes during Human Cytomegalovirus Infection is Dependent on IRF3 Expression Viruses. 2019 Mar 12;11(3):246.doi: 10.3390/v11030246. Authors

Are there any ISGs that are dependent on IRF3?

Several ISGs, including IFIT1, IFIT2, IFIT3, Mx1, Mx2, CXCL10 and ISG15 were found to be upregulated transcriptionally following HCMV infection independently of type I IFN-initiated JAK-STAT signaling, but dependent on intact IRF3 signaling.

How is the TLR4 / IRF3 pathway activated by pathogens?

This TLR4/IRF3 pathway of pathogen discrimination was activated by ceramide and by P-fimbriated E. coli, which use ceramide-anchored glycosphingolipid receptors.

What happens to IRF3− / − mice after E coli?

Following uropathogenic E. coli infection, Irf3−/− mice showed a pathogen-specific increase in acute mortality, bacterial burden, abscess formation and renal damage compared to wild type mice.