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Hi, I'm Dr. Janet Pope, or tweeting as Janet Burdope.
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I'm here at RheumNow at ACR 2026 in Orlando, Florida.
0:15
I wanted to talk about SNIPS and snippets and interstitial lung disease related to our SARDs.
0:20
So I'm going to talk about three posters: 0019, 0037, and 0025, and they have some mechanisms of action in common and different pathways.
0:33
So the first one, 0019, was looking at TL1A in sarcoidosis and looking at the fibrosis in sarcoidosis, which could be systemically all over, including in the lungs.
0:48
TL1A is a target for some drug trials for pulmonary interstitial lung disease.
0:52
So what they found was TL1A was abnormal in the myeloid cells and eventually in the cells that became and made granuloma.
1:02
And so it would look like it's something important in causation.
1:06
What they found was TL1A was affecting TNF, IL-1 beta, IL-6, and IL-17.
1:12
And they're all cytokines we're very familiar with in inflammatory arthritis, as a for instance.
1:18
So I think this might mechanistically give us an idea of upstream and downstream areas for interstitial lung disease or fibrosis that we might be able to target.
1:28
The next one was looking at poster 0037, and it was looking at scleroderma.
1:37
They wanted to look at correlations with baseline FVC, so forced vital capacity, and it was actually FVC% predicted.
1:44
So they did a whole array on 60 patients with scleroderma and 19 with scleroderma with no ILD, and they kind of matched those patients.
1:56
What they found was predictive at baseline but not a worsening over time.
1:59
So both an elevated KL-6 and an abnormal ICAM-1 were both important for low FVC at the beginning.
2:08
However, the holy grail in scleroderma is predicting who might have upregulated things that might actually show that we can predict what's going to happen in scleroderma.
2:23
The final one was from UCSF. It's 0025, and it was looking at some similarities, comparing and contrasting SARDs and progressive pulmonary fibrosis including IPF.
2:37
So it's been known — and I guess now to me as well — that short telomeres are a big deal in IPF, that they're often present, and I think they're correlated with worse IPF, and some people are even ordering telomeres more for research purposes.
2:55
So what they wanted to look at was senescence with epithelial remodeling — that would be bad remodeling.
3:02
What they found was that DNA damage was quite common in the patients with ILD and the SARDs, the systemic autoimmune rheumatic diseases, and also in IPF.
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Why did I choose this poster? Because I think it's yet another pathway to say: if there's abnormal senescence, are there ways of changing that that we could modify or decrease the chance of someone with a SARD going to fibrosis.
3:27
So I hope these snippets that I got from posters will be helpful to you in understanding of the SARDs. Thank you.
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