Joint Ventures: CAR-T, Early Diagnosis Reshape Scleroderma at EULAR 2026

And obviously you're on, so I have to ask you about scleroderma.

So what have your highlights been so far?

Yeah, so, I mean, speaking first about some of the abstracts and the poses that I've seen, what we are seeing, I think, recently, which has already been there in your field, lupus, non-niscleroderma comes secondary to lupus, so what we're seeing, we're always there and learning from you guys.

So we can see a bit of a paradigm shift now.

Whereas before, treatments used to be based on the fibrotic aspects of the disease, what people could see.

So your CT scans, you've got your fibrosis, your skin's affected, you've got digital ulcers.

And those are the things that used to be treated, of course.

But now, with recent literature evidence that actually these biomarkers that we suspected, these autoantibodies, you know, anti-TOPR isomerase or only Pol-3 or whatever you want to speak about, actually potentially are not just biomarkers.

And we're actually seeing that there's potential disease being driven through there with evidence of mitochondrial damage leading to disease effects and also anti-TOPR isomerase entering cells.

So it's gone from that shift from it's not just a biomarker, but actually it's an auto antibody-driven disease, which is a different concept of looking at it.

And there has been previous work looking at rituximab having effects on B cells and the positive trials there.

So just out of one paper that we saw was an Italian group where they've shown dual therapy, so with rituximab and mycophenolate, showing better outcomes on skin and lung as well, rather than just monotherapy in each one.

But as you know well, you know, rituximab is just working on CD20, and it's not working on those long-lived plasma cells.

So now obviously we start talking about CAR T, But what's one step further in this Congress, which I came across, was a Chinese group by Zhang Getong, where they're not just looking at the CDM-19 aspect of CAR-T, but also BCMA, which is the BISO-activating factor, one of the receptors, one of the BAS receptors.

And what they've shown is this concept of immunological reset, which is obviously a concept, you know, your team with Ed in Leeds is already, you know, I've gone into previously where, you know, you are not just getting rid of that CD19, but you're also resetting it with the BCMA.

So what the group found is a proof-of-concept study.

What they found was that you are getting a reduction in antibodies, including antitopor isomerase as well.

So what they found is that with that reduction, if we are thinking that this is now an autoantibody disease-driven condition, that we've got a potential starting point.

you know granted it's it was a small study nine patients

yeah

but it's a it's a start

you know

yeah and it's building and they've also because obviously um contrary to lupus and you've got the added fibrotic milieu in scleroderma so they've actually tried to optimize the cartoon a separate uh abstract that we've got in the conference here where they've used edta to collate the fibrotic components in the tissue, which also lead to more efficacy of the CAR-T. It's a very interesting area of scleroderma now that we're entering, and as I mentioned, the paradigm shift that we're seeing now.

Yeah, and it's interesting, isn't it, because it's things learned that have been demonstrated in lupus.

We're copying each other's homework in that sense, which is helpful from that point of view.