Professor Luke O'Neill

And they turn over.

All cells in our body turn over and they die and are replaced.

In psoriasis, it's very simple.

They're dividing too much and they reckon overall they're dividing about three times the rate in normal skin.

And they pile up and they pile up and they pile up in the skin and they die and then debris is formed and the immune system doesn't like this and it goes in and tries to handle this situation.

And the trouble is that immune reaction then causes all the features of an immune type response.

You get redness, you get itchiness, you get pain, just as if you've scratched yourself, I suppose, in a way.

And in this case, the scratch is being caused by your own cells in your skin dividing too much.

In some ways, we see most autoimmune diseases, they're sometimes called wounds that won't heal properly.

Because you can imagine if you scratch yourself in the skin, it will go red, it will be sore.

The immune system will go in and try to clear sort of any infection that's in the broken skin.

That's what's happening in psoriasis, but there's no infection.

That's the mystery.

Why would the immune response be kicked off in that situation and mimic as if there's been an injury and infection?

And that's the thing we don't know.

and begin to irritate further.

But it's very hard to find a bacteria in the skin of psoriatic people.

And so it's been caused by that.

If it was caused by a bacteria, of course, it would respond to antibiotics.

And it doesn't really, mostly speaking.