​Study finds soluble CD13 higher in patients but not tied to severity
Written by Marisa Wexler, MS | February 17, 2026

Levels of soluble CD13, the circulating form of a protein involved in inflammation and fibrosis (scarring), are generally higher in people with scleroderma, but do not clearly correlate with disease severity or specific clinical features, a new study reports.

The findings suggest that CD13 alone is unlikely to serve as a reliable standalone biomarker for scleroderma, though more research is needed to understand whether it may help track how the disease changes over time.

The study, “Soluble CD13 in systemic sclerosis: clinical observations and transcriptomic insights from peripheral blood,” was published in Arthritis Research & Therapy. 

What scleroderma is and why CD13 may be involved
​Scleroderma, also called systemic sclerosis or SSc, is a disease marked by inflammation and fibrosis that can affect the skin and internal organs. The causes of scleroderma are still not completely understood.

CD13 is a signaling protein known to help regulate inflammation and fibrosis. In this study, the researchers examined whether blood levels of soluble CD13 (sCD13) are altered in people with scleroderma and whether they correlate with SSc subtypes, blood vessel complications, skin and lung fibrosis, or SSc-specific autoantibodies — immune proteins that mistakenly attack the body’s own tissues.

The researchers first analyzed plasma CD13 levels in 30 people: 10 with limited scleroderma, 10 with more severe diffuse scleroderma, and 10 healthy individuals. The groups were matched for factors such as age and sex. Here, the researchers found that CD13 levels were significantly higher in participants with diffuse scleroderma than in those with limited disease, but neither group showed significantly higher levels when compared with healthy controls.
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In a larger group designed to evaluate blood vessel complications, blood levels of CD13 were significantly higher in people with scleroderma than in controls, but no difference was seen between disease subtypes. Likewise, in a third group of patients with early-stage scleroderma, CD13 levels were again elevated compared with controls, but did not differ between disease subtypes.
“Altogether, significant elevation of sCD13 in SSc patients compared to healthy controls was consistently observed, however there was no difference between disease subtypes,” the team wrote.

PD-1 receptor ID'd as target for slowing disease progression
Written by Steve Bryson, PhD | February 10, 2026

​Mesenchymal stem cells (MSCs) — a type of regulatory cell found in various tissues — work to reduce lung scarring in systemic sclerosis (SSc) by suppressing the growth of certain immune T-cells that carry the PD-1 receptor, according to a new study.

PD-1 is an immune checkpoint protein receptor found on T-cells that normally functions to prevent overactive immune responses and autoimmunity. In SSc patients, however, a subset of T-cells that carry PD-1 appears to drive disease progression, particularly in SSc-related interstitial lung disease (SSc-ILD), the data suggested.
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“These findings highlight PD-1 as a therapeutic target and support the clinical investigation of MSC-based interventions for SSc-ILD,” the researchers wrote.
Their study, “Mesenchymal stromal cells ameliorate systemic sclerosis-interstitial lung disease via PD-1/PD-L1 signalling axis,” was published in the journal RMD Open.

Targeting macrophages could be effective in disease prevention written by Marisa Wexler, MS | February 3, 2026

Macrophages, a type of immune cell, may be mainly responsible for driving fibrosis, or scarring, in people with scleroderma, according to new research done in animal models.

“These data suggest that a single cell type, macrophage, may be responsible for inducing scleroderma,” Sanja Arandjelovic, PhD, who co-led the study at the University of Virginia, said in a university news story. “Although more research is needed on understanding whether targeting these cells later during disease progression can reverse the existing tissue damage, our data suggest that macrophage inhibition could be effective in disease prevention in the high-risk patient population.”
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The study, “Macrophages Are Critical Inducers of Bleomycin-Induced Fibrosis in a Systemic Scleroderma Model,” was published in The American Journal of Pathology.

Researchers ID 3 genes that were significantly dysregulated in SSc patients
Written by Steve Bryson, PhD | January 27, 2026

Abnormal fatty acid metabolism may play a role in the development of systemic sclerosis (SSc), according to a gene activity analysis.

Researchers identified three genes involved in fatty acid metabolism that were significantly dysregulated in SSc patients. These changes correlated with markers of fat metabolism and disease complications, including lung involvement, the data suggested.
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These findings indicate that “dysregulated fatty acid metabolism may be implicated in the [development] of SSc,” which may provide “potential targets for metabolic intervention,” researchers wrote in the study, “Expression and clinical significance of fatty acid metabolism–related genes in PBMCs of SSc patients,” which was published in Clinical Rheumatology.