
In a hospital in Sweden, surgeons made a small cut in a man’s forearm and injected millions of tiny clusters of donor cells. The 42-year-old had lived with type 1 diabetes for nearly 40 years, his body unable to make insulin. These genetically engineered cells were designed to restore that ability without provoking the immune attack that had destroyed his own.
Four months later, the cells were still working, producing insulin with no need for immune-suppressing drugs.
Making Donor Cells Invisible to the Immune System
Type 1 diabetes occurs when the immune system mistakenly destroys beta cells in the pancreas, which produce insulin. For decades, scientists have tried replacing those cells with ones from donors. The approach works—but only if patients take lifelong immunosuppressants, which raise the risk of infections, cancer, and other serious problems.
The new study, led by Uppsala University Hospital and published in The New England Journal of Medicine, tested a radically different strategy: instead of weakening the immune system, hide the transplanted cells from it.
Scientists started with insulin-producing islet cells from a donor pancreas. Using a gene-editing tool called CRISPR-Cas12b, they switched off two genes that make proteins telling the immune system a cell is “foreign.” Then they increased a protein called CD47—a.k.a. the “don’t eat me” signal—so the body’s immune cells would be less likely to attack.
The result was a “hypoimmune” cell—one that neither the adaptive nor innate immune system should recognize as a threat.
A First Human Example
The man received 79.6 million of these modified cells, injected into 17 tiny tracks in his forearm muscle. No steroids, no anti-inflammatory agents, no immunosuppressants.
Over the next 12 weeks, his doctors monitored him closely. The unmodified and partially edited cells in the transplant were quickly destroyed, sparking strong T-cell and antibody responses. But the fully edited hypoimmune cells escaped notice entirely.
“We did not detect any immune response targeting the HIP (hypoimmune) islet cells over the course of the study,” the authors wrote.
The surviving cells made insulin, shown by steady C-peptide levels that rose after meals—a sign they were working. His average blood sugar levels, measured by HbA1c, fell by about 42%. He still needed daily insulin, which was expected, since the transplant provided only a small fraction—around 7%—of the amount needed for full replacement.
Imaging scans showed the grafts were alive and well, without inflammation. Four mild side effects occurred, none related to the transplanted cells.

Encouraging Signs, More to Learn
This was a single-patient proof-of-concept, aimed at showing safety and feasibility rather than a cure. The researchers say the next steps will involve higher doses and longer follow-up to see if insulin independence is possible.
While the work is early, it builds on years of animal experiments showing that hypoimmune cells can survive without immune suppression in mice and monkeys. It also hints at a broader future: the same genetic strategy could, in theory, protect other transplanted tissues and organs from rejection.
For millions living with type 1 diabetes, the idea of a curative cell transplant without dangerous drugs has been a distant hope. Now, with a small incision in a forearm and some precisely edited cells, that hope has taken a tangible step forward.