Platelets and platelet adhesion pathways at the islet–blood interface (IBMIR)

The Platelets and platelet adhesion pathways at the islet–blood interface refers to the Instant Blood-Mediated Inflammatory Reaction (IBMIR), a rapid thromboinflammatory response triggered when isolated pancreatic islets are infused into the portal vein during clinical islet transplantation (Bennet et al., 2000, Diabetes). This reaction is initiated by the expression of Tissue Factor (TF) on the surface of the transplanted islets, which activates the extrinsic coagulation pathway and leads to the rapid recruitment and activation of platelets (Moberg et al., 2002, Lancet). Activated platelets adhere to the islet surface via receptors such as P-selectin and GPIIb/IIIa, forming a fibrin-rich clot that entraps the islets and promotes the infiltration of inflammatory leukocytes (Nilsson et al., 2007, Xenotransplantation). This process results in significant early islet destruction, reducing the mass of functional beta cells available to achieve insulin independence in patients with Type 1 diabetes. Therapeutic interventions target various components of this pathway, including the use of anticoagulants like heparin or low molecular weight dextran sulfate, and anti-platelet agents like abciximab to mitigate graft loss (Johansson et al., 2005, Diabetes). Managing these pathways is critical for improving the survival and long-term function of transplanted islets.

Other names

Instant Blood-Mediated Inflammatory ReactionIBMIRIslet-blood interface adhesionPlatelet-islet interactionThromboinflammatory reaction in islet transplantation

Inhibition of platelet activation and aggregation, suppression of the coagulation cascade, and blockade of complement-mediated inflammation at the islet surface to prevent the Instant Blood-Mediated Inflammatory Reaction (IBMIR).