IRA FLATOW: This is Science Friday. I’m Ira Flatow. If you’ve ever suffered from eczema or psoriasis, you know the feeling when an attack is coming on. You can feel the irritation, the swelling, the onslaught your immune system is about to launch against your skin. And there’s not much you can do about it at that very moment.

But now scientists have designed a type of cellular implant that listens for those first rustlings of an imminent attack. And the cells actually launch their own counterattack of anti-inflammatory compounds. How do they do it? Well, that’s what we’re going to be talking about. Martin Fussenegger is a senior author on that research out this week in the journal Science Translational Medicine. He’s also a professor of biotechnology and bioengineering at the Swiss Federal Institute of Technology. That’s in Zurich, Switzerland. Welcome to Science, Friday.

MARTIN FUSSENEGGER: Yeah, hi, Ira, good afternoon.

IRA FLATOW: Good– thank you, good evening to you.

MARTIN FUSSENEGGER: Thank you.

IRA FLATOW: Tell us how these designer cells work. How do they stop the psoriasis from flaring up?

MARTIN FUSSENEGGER: Well, what we’ve done is we’ve taken human cells that were put into culture a long time ago and we have equipped these cells with genetic circuitry that can sense the primary proteins of immune system that trigger psoriasis. And these design cells can not only sense psoriasis and its components, these pro-inflammatory proteins, they can also process that information and choose an appropriate response to stop psoriasis. And they do that by producing specific proteins which are also cytokines, but this time anti-inflammatory cytokines. They are produced by the designer cells, secreted by them, and delivered back into the bloodstream, where they contain and shut down the inflammation.

IRA FLATOW: And you’ve tried this out in mice in the laboratory.

MARTIN FUSSENEGGER: Yes, exactly. We have designed human cells, as I just mentioned. We’ve packaged them into alginate beads, that’s an algae gelatin sugar structure, such as to protect the human cells and the human componentry from the mouse immune system.

IRA FLATOW: And it works?

MARTIN FUSSENEGGER: Yes, it works. So if we induce psoriasis in those animals– we do that by just shaving them and applying a specific cream that triggers a massive inflammation of the skin, which is almost identical to a psoriatic flare in humans. And we could show that mice which have been implanted with those designer cells, they did not get a psoriatic flare. Because the designer cell was early on detecting that immune system is mounting an inflammatory response and were just shutting it off from the beginning. So psoriasis could not even develop.

IRA FLATOW: So how do we move this into people?

MARTIN FUSSENEGGER: Well essentially we’re already rather close, because we’re using human cells, we’re using human componentry, and we’re using human anti-inflammatory proteins, those cytokines, which have already been tested in human clinical trials. So what we would do next is we need to bring several people together, because we cannot carry this forward without scientists and a public research institution. We’re engineers. We need to team up with medical doctors at the university hospitals.

We also need to have far more people at the table. And these three different groups will develop that further, with the first steps being to produce these human designer cells under what we call good manufacturing practice– GMP– which is a standard protocol issued by the authorities, protocols which you need to follow when you would like to go with biological material into patients.

IRA FLATOW: Would this be something you slip under the skin of people with psoriasis?

MARTIN FUSSENEGGER: Exactly. We would package it in, not necessarily in this algae gelatin, although this material has been already licenced for clinical trials. We would put that into a plastic bag, which is what we called semi-permeable, which means the immune system will not attack the cells, yet the psoriatic cytokines can go to the designer cells and the designer cells can react to contain psoriasis. And we would put that under the skin, where the designer cells automatically connect to the bloodstream, so they can detect the onset of psoriasis and can produce and systemically deliver the anti-inflammatory proteins.

IRA FLATOW: Could this theoretically, this kind of treatment, be used for other inflammatory diseases like arthritis or autoimmune diseases?

MARTIN FUSSENEGGER: Yes, exactly. The principle is kind of generic, because we could exchange the sensor capacity of these designer cells. Instead of just sensing the two cytokines that are so specific for psoriasis, we would exchange them to send some molecules for other autoimmune diseases. And then, again, the processing capacity could be the same. And in case we needed to produce anti-inflammatory proteins, this could all go into the same concept and could also be designed for other auto-inflammatory diseases and autoimmune diseases.

IRA FLATOW: This is a long process. When we talk about cures or treatments, people who have the diseases, or everybody knows somebody who knows somebody who has something like this, they said, when can I have this. You’re talking about years from now, right?

MARTIN FUSSENEGGER: Yeah. I think this will certainly take 10 years from now on. And this may be a disappointment for some. But I think it’s very important.

This is a completely new treatment strategy which has not been tested before. And safety’s always first. We don’t want to rush this on the market at the risk of harming the patients.

We would like to offer a new treatment concept for psoriasis and beyond. And this needs to be carefully tested according to the rules. And I believe we’re getting there, but it’s not an immediate product that people can expect in the next two, three years. I think this will take 10 years.

IRA FLATOW: Well, Dr Fussenegger, we wish you good luck. And we’ll hope to follow this along with you. Martin Fussenegger, professor of biotechnology and bioengineering at the Swiss Federal Institute of Technology. That’s in Zurich, Switzerland.

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