Researchers at Koç University report that disabling candidate genes RNLS or HIVEP2 does not suffice to prevent rejection of transplanted pancreatic beta cells, underscoring challenges in immune protection for diabetes therapies.
Gene editing has fallen short in a new attempt to shield transplanted pancreatic beta cells from immune attack, according to researchers at Koç University. Their work suggests that disabling either of two candidate genes, RNLS or HIVEP2, does not by itself give transplanted cells enough protection to survive rejection in diabetes models. (news-medical.net)
Type 1 diabetes develops when the immune system destroys beta cells, which normally produce insulin. Replacing those cells remains one of the most promising ways to restore the body’s own insulin production, but transplanted tissue is often attacked quickly unless patients take long-term immunosuppressive drugs, which can raise the risk of infection and some cancers. (news-medical.net)
In the Koç University study, researchers used CRISPR-Cas9 to switch off RNLS and HIVEP2 separately in mouse and human beta-cell lines, then formed the edited cells into three-dimensional spheroids that more closely resemble pancreatic islets. Before transplantation, the team found that HIVEP2 loss did not materially affect beta-cell function, while RNLS loss caused only a modest drop in glucose-stimulated insulin release in mouse cells. (news-medical.net)
The edited spheroids were transplanted under the skin of immune-competent mice and tracked with bioluminescence imaging. Neither genetic change extended graft survival, and both mouse and human cells were eventually rejected at about the same rate as unedited controls. The finding comes against a broader backdrop of progress in the field: studies published in the New England Journal of Medicine in 2025 reported early success with gene-edited islet transplants in people with type 1 diabetes, while recent reviews have argued that more durable solutions will probably need several genetic changes, or a mix of gene editing and immune-modulating biomaterials. (news-medical.net)
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