Cytotoxic T cell

I put together this table really to set the stage on the biological distinction across molecules and therapeutic implications.

I want you to think about different points, checkpoint coverage, cellular binding site, CD8, CD28, CTLA-4 networks.

We're really going through basic biology to set the stage for clinical practice and preserved inhibitory signaling.

And I want you to look at those in the context of PD-1 and PD-L1 VEGF.

And so that justified the hypothesis and the data that we have around VEGF neutralization and neutralization.

This is another very important point if we think about basic biology justifying therapeutic implications.

The PD-1 VEGFA molecules do not directly disrupt the PD-L1 CD8 complexes.

In the context of PD-L1 VEGFA, we might have disruption of these complexes, but we do not have inerrant CD8 co-stimulation gain.

I put together this table really to set the stage on the, um, biological distinction across molecules and therapeutic implications.

Uh, I want you to think about different points, checkpoint coverage, cellular binding site, um, CD8, CD28, CTLA4 networks.

We're really going through basic biology to set the stage for a clinical practice and a preserved, uh, inhibitory signaling.

And I want you to look at those in the context of PD-1 and PD-L1 VEGF-A blockade.

And this is a very important point, uh, because here the checkpoint arm can influence where the molecule is retained, and so that justified the hypothesis and the data that we have around VEGF neutral-- its localization and neutralization.

This is another very important point if we think about basic biology justifying, um, therapeutic, uh, implications.

Uh, the, uh, PD-1 VEGF-A, uh, molecules do not directly disrupt the PD-L1 CD8 complexes.

Uh, in the context of PD-L1 VEGF-A, um, we might have disruption of these complexes, uh, but we do not have, uh, inherent CD8, uh, co-stimulation gain.

I put together this table really to set the stage on the biological distinction across molecules and therapeutic implications.

I want you to think about different points, checkpoint coverage, cellular binding site, CD8, CD28, CTLA-4 networks.

We're really going through basic biology to set the stage for clinical practice and preserved inhibitory signaling.

And I want you to look at those in the context of PD-1 and PD-L1 VEGF.

And so that justified the hypothesis and the data that we have around VEGF neutralization and neutralization.

This is another very important point if we think about basic biology justifying therapeutic implications.

The PD-1 VEGFA molecules do not directly disrupt the PD-L1 CD8 complexes.

In the context of PD-L1 VEGFA, we might have disruption of these complexes, but we do not have inerrant CD8 co-stimulation gain.

I put together this table really to set the stage on the, um, biological distinction across molecules and therapeutic implications.

Uh, I want you to think about different points, checkpoint coverage, cellular binding site, um, CD8, CD28, CTLA4 networks.

We're really going through basic biology to set the stage for a clinical practice and a preserved, uh, inhibitory signaling.

And I want you to look at those in the context of PD-1 and PD-L1 VEGF-A blockade.

And this is a very important point, uh, because here the checkpoint arm can influence where the molecule is retained, and so that justified the hypothesis and the data that we have around VEGF neutral-- its localization and neutralization.

This is another very important point if we think about basic biology justifying, um, therapeutic, uh, implications.

Uh, the, uh, PD-1 VEGF-A, uh, molecules do not directly disrupt the PD-L1 CD8 complexes.

Uh, in the context of PD-L1 VEGF-A, um, we might have disruption of these complexes, uh, but we do not have, uh, inherent CD8, uh, co-stimulation gain.

I put together this table really to set the stage on the, um, biological distinction across molecules and therapeutic implications.

Uh, I want you to think about different points, checkpoint coverage, cellular binding site, um, CD8, CD28, CTLA4 networks.

We're really going through basic biology to set the stage for a clinical practice and a preserved, uh, inhibitory signaling.

And I want you to look at those in the context of PD-1 and PD-L1 VEGF-A blockade.

And this is a very important point, uh, because here the checkpoint arm can influence where the molecule is retained, and so that justified the hypothesis and the data that we have around VEGF neutral-- its localization and neutralization.

This is another very important point if we think about basic biology justifying, um, therapeutic, uh, implications.

Uh, the, uh, PD-1 VEGF-A, uh, molecules do not directly disrupt the PD-L1 CD8 complexes.

Uh, in the context of PD-L1 VEGF-A, um, we might have disruption of these complexes, uh, but we do not have, uh, inherent CD8, uh, co-stimulation gain.

We give it a code for every HLA type the immune system's got.

We give it a code for every mutation it's got, and we ask it to predict now what's the CD8 response or the likelihood of a T cell reacting to it.

And if we train that over many, many patients in parallel, it can make a prediction.

And these predictions are looking really interesting because most of them validate what we already know, but some of them are new.

in lesional skin, acting very early as an alarming upon epidermal injury.

So now what's the role of this IF33? So we all know that, and it has been well described, that CD8-close T cells are the main killers in epidermal necrolysis.

And we have shown that when we expose CD8 T cells from patients with epidermal necrolysis to IF33 in combination with interferon gamma, that is also highly released in this condition.

And these CD8 T cells become more cytotoxic.

They upregulate cytolytic molecules.

So there is a boost of the cytotoxic response due to the presence of IL-33.

So there is a kind of pathogenic loop.

So damaged keratinocyte release this alarmine, and this alarmine then boosts the CD8 response.