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Data · dataset · 2026

<b>Microgels Containing Protease Resistant CXCL12 and FasL Enable Long Term Allo-Islet Function Without Systemic Immunosuppression</b>

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<p dir="ltr">Type 1 diabetes (T1D) is a chronic disease characterized by the autoimmune destruction of insulin-producing beta cells in the pancreas.

Description

Replacement of beta cells by islet transplantation has proven to be successful in providing a functional cure for T1D. We have previously shown that microencapsulation of allo or xeno-islets with CXCL12 promotes beta cell function, provides immune protection, and facilitates vascularization at the graft site in both small and large animal models of T1D.

In addition, streptavidin-Fas Ligand (SA-FasL) microgels have been shown to induce immune acceptance of allogeneic islets through expansion of T regulatory cells (Tregs) in combination with short-term systemic immune suppression. This study evaluated a combination of these two complementary approaches for extending allo-islet graft survival in a mouse model of T1D through the co-delivery of SA-CXCL12 or a protease-resistant variant of the chemokine (SA-prCXCL12) and SA-FasL within biotinylated microgels in an allogeneic transplant setting.

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We demonstrated that microgels coated with SA-FasL and SA-prCXCL12, when co-transplanted with allogeneic islets, sustained long-term (6 months) diabetes reversal in STZ-treated mice without any systemic immunosuppression more effectively than either agent alone. Our findings demonstrate in this murine model of diabetes that microgels delivering a combination of SA-prCXCL12 and SA-FasL induces long-term local immune protection of the allo-islet graft, enhances intragraft Treg recruitment and improves graft vascularization while abrogating the need for any systemic immune suppression.</p>

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Disease 75%
Provenance · 1 source records, 9 field assertions
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ZivaHuboai:figshare.com:article/3336908813 d agoJSON v1
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