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Genetically engineered stem cell-derived islets that express the chemokine CCL22 have been developed to improve outcomes after islet transplantation for type 1 diabetes. By secreting CCL22, these islets recruit regulatory T cells (Treg) to the transplantation site via C-C motif chemokine receptor type 4 (CCR4), promoting a tolerogenic immune environment. This approach aims to reduce both allo- and autoimmune attacks against the transplanted insulin-producing β cells, potentially reducing or eliminating the need for chronic immunosuppression. In preclinical models, these CCL22-expressing SC-islets retained normal function and were effective in attracting Treg, enhancing graft survival and β cell function in diabetic mice[3][1][5].
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