Dr. Kevin Tracey

It's great to be here, Eric.

Thank you for having me on.

I'm looking forward to this chat with you.

It is.

It is a fair summary of what happened.

Back in the 80s, I was part of the team here in a few blocks from where I'm sitting in New York City at Rockefeller and Cornell that identified the biological activity of TNF as a major mediator.

He first demonstrated that monoclonal antibodies...

targeting TNF could inhibit inflammation.

Now, this was published back in Nature in 1987 in a paper I wrote with my colleagues.

And this paper was the first description of monoclonal anti-TNF antibodies as having a therapeutic potential.

And of course, today, those antibodies have all kinds of commercial names like Humira and Remicade and

and they're related ones for IL-1.

And we call the whole thing cytokine storm.

But back when we were doing this work, what we were actually defining was that TNF is sort of the proximal trigger of a cytokine storm.

And today that's treated with these monoclonal antibodies.

But the real question that remained is if the body has the ability to produce these molecules, cytokines, TNF, other things, that can cause so much damage through inflammation,

then how is it normally controlled?

What is it that evolution did over millions of years to put the brakes on inflammation and prevent it from causing damage in most of us who are healthy?

And that question led to the discovery of the rule of the vagus nerve acting like the brakes on your car to suppress inflammation.

So the holy shit moment came in the 1990s.