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Causes & What We Know/July 10, 2026/2 min read

A New Target in the Search for Type 1 Diabetes Prevention

Researchers have identified a marker that appears on harmful immune cells in Type 1 diabetes, and early evidence suggests targeting these cells could prevent the disease without suppressing the entire immune system.

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Key takeaways

  • CD38 is a protein marker found on T cells that appear to drive Type 1 diabetes development
  • In laboratory and animal studies, selectively removing CD38-expressing cells prevented diabetes onset
  • This approach preserved protective immune cells called Tregs, unlike current broad immune-suppressing therapies
  • The research is in early stages and has not yet been tested in patients

The Challenge with Current Approaches

Type 1 diabetes occurs when the immune system mistakenly attacks insulin-producing beta cells in the pancreas. While some T-cell depleting therapies can delay progression of Type 1 diabetes, they come with a significant drawback: they suppress many types of immune cells all at once, including regulatory T cells (Tregs) that actually help maintain immune tolerance and prevent autoimmune disease.

Researchers have been searching for ways to stop the harmful immune attack without disarming the entire immune system. A new study suggests they may have found a more precise target.

Identifying CD38 as a Pathogenic Marker

Scientists studied non-obese diabetic (NOD) mice, which naturally develop a diabetes-like disease, and blood samples from recently diagnosed Type 1 diabetes patients. In both, they found that CD38—a protein on the cell surface—marked a specific population of T cells that appeared to drive the autoimmune attack on beta cells.

Using animal models, the researchers demonstrated that T cells expressing CD38 were capable of causing diabetes when transferred to other mice. This evidence suggested that CD38+ T cells were central to the disease process.

A More Selective Approach

The team tested whether selectively removing CD38-expressing cells, using an engineered antibody (anti-CD38 monoclonal antibody), could prevent diabetes. In both a standard mouse model and a humanized mouse model designed to mimic human autoimmune diabetes, the treatment prevented both insulitis (immune attack on islets) and diabetes onset.

Importantly, this selective depletion preserved CD4+ CD25+ Tregs—the protective immune cells that broader therapies typically eliminate. The anti-CD38 approach did not appear to harm islet function, and may even eliminate senescent beta cells that were already damaged or contributing to immune activation.

What This Means and What Comes Next

These results suggest that targeting CD38+ autoreactive T cells could represent a new strategy for preventing or slowing Type 1 diabetes by removing the specific cells driving the autoimmune attack while preserving immune tolerance. The approach is appealing because it is more targeted than current therapies.

This is fundamental research, conducted in animal models and analyzing patient blood samples. Human clinical trials would be needed to determine whether this strategy is safe and effective in people with Type 1 diabetes or at high risk of developing it. Researchers and clinicians will be watching for the next stages of this investigation.

Evidence label

Source: bioRxiv : the preprint server for biology. Evidence type: PubMed indexed literature. Type1Cure is an information and intelligence hub, not a medical advice service. This article summarizes published research and does not provide diagnosis, treatment, or personal medical guidance. Always talk to your own care team before changing anything about your Type 1 diabetes management.

Type1Cure is an information and intelligence hub, not a medical advice service. This article summarizes published research and does not provide diagnosis, treatment, or personal medical guidance. Always talk to your own care team before changing anything about your Type 1 diabetes management.

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