Polly Matzinger Recaps 65 Years of Immunological Theory in One Diagram
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- Опубліковано 5 вер 2016
- Polly Matzinger, of the National Institute of Allergy and Infectious Diseases, presents on the Danger Model at the OHTN Back to Basic research conference in Toronto. In this section of her presentation, Polly uses overhead projection to illustrate major developments in immunological theory over the past 65 years.
For more information and resources, visit backtobasic.ohtn.on.ca/
For a descriptive transcript of this video, visit: www.ohtn.on.ca/polly-matzinger... - Наука та технологія
I'm attempting to work in a fault detection system inspired by the immune system (Artificial Immune Systems - AIS), and stumbled upon this video. Matzinger is a name I had previously read on papers regarding immunology while trying to understand AIS solutions in both self/non-self vs danger theory scenarios. Damn, are you good at explaining these concepts! I'm an engineer, not an immunologist, but I understood it all, good job!
PS: That American cop critic at the end, though. Who would've guessed it would age so well!
Well said! Clarity in scientific presentations is rare
A really great talk! Dr. Matzinger clarified so many confused definitions so clearly. It helped me a lot.
Bravo, incredible presentation!
hey hey people!
I'm quite new to the field of immunology and currently I have to deal with the topic self/non-self vs danger model. Recently, I dealt with the fetomaternal tolerance. Here's what I learned:
Trophoblast cells lack classical MHC2 molecules and instead express non-classical HLA-G and HLA-E to be safe from NK cells
. Placental trophoblast cells produce cytokines that limit Th cell activation (IL-10, TGF-β) and help to expand Tregs (iTreg, they also act immune suppressive through IL-10). Then there is the
decidua that represses the local expression of T cell-attracting chemokines. So collectively both, maternal and fetal factors, contribute to the formation of an immunologically privileged site.
How do those findings fit into the danger model? To me it looks like both, the fetus and the mother, activly prevent a maternal non-self response.
Have you found out?
I guess according to the danger model, fetuses are just not dangerous enough to trigger an immune response. When they shape their fingers, they use apoptosis. No danger signals are emitted... However, there is foreign material. And here is the molecular pendant to your statement. In the placenta, there is an enzyme, IDO1 which breaks down tryptophane to kynurenines by oxidatively cracking open the indole ring of the tryptophane. Problem is, T-Cells need this tryptophane. So they can not pass the placenta where this enzyme is active which is degrading it Tumors sometimes also produce IDO1. Plus it can be triggered by IFN-gamma (and other cues)... pubmed.ncbi.nlm.nih.gov/12385839/
How do u define mechanism of action under danger model for vaccine for which dead virus bacteria used ,
She’s a legend but it is not some theoretical speculation, immunological theory is heavily backed up by results.