Hi. This is Seth Masters from the Walter and Eliza Hall Institute.
Today, I'm going to be discussing "Cytoplasmic Innate Immune Sensors".
Specifically, we'll start with a discussion
of the adaptive and the innate immune systems,
comparing and contrasting them with examples of autoinflammatory and autoimmune disease.
I'll then proceed to discuss individual cytoplasmic innate immune sensors and use some of
these autoinflammatory diseases to explain how each of
these cytoplasmic innate immune sensors work in context.
Finally, I will finish by discussing some additional concepts,
which I hope bring the field together and link some of
these different NLRs together in a conceptual framework.
So to begin, autoinflammatory syndromes or otherwise known as periodic fever syndromes,
were initially described as genetically inherited,
unprovoked, systemic inflammatory diseases.
These stemmed from the fact that they had no predilection towards autoimmunity i.e,
no antigen specific T-cells,
no high-titer autoantibodies, and in contrast,
there was a very strong activation of innate immune cells.
So these are things like neutrophils and macrophages, for example.
That is what spawned the necessity
of distinguishing the autoinflammatory diseases from the autoimmune.
And I think that it sets itself up as a very nice dichotomy,
where in both cases,
you have activation of the immune system,
but for autoimmune diseases,
you have activation of the adaptive immune system,
whereas in autoinflammatory diseases,
you have activation of the innate immune system.