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Blood-Mediated Inflammatory Reaction (IBMIR) and Prevention of IBMIR

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Glycoimmunology in Xenotransplantation
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Abstract

In transplantation, function loss of grafts is primarily observed in the early time of transplantation, mainly by two known responses of the instant blood-mediated inflammatory reaction (IBMIR) and hyperacute rejection (HR) [1]. It was reported that the first few hours have been reported to display the IBMIR after cell infusion of xenoantigenic islets [2]. IBMIR is characteristic of innate inflammatory responses and thrombotic pathway displayed by a serial reaction complement activation, immune cell infiltration, platelet adhesion, and coagulation [3]. IBMIR is frequently coupled with thrombosis and releases inflammatory mediators such as monocyte chemoattractant protein-1 (MCP-1), macrophage migration inhibitory factor (MIF), and IL-8. Thrombin fundamentally activates platelets. In addition, thrombin can activate innate immune cells of monocytes and neutrophils. Islets-producing tissue factors mainly cause the IBMIR as a causing factor [2, 4]. Therefore, the thrombosis reaction is prevented by blocking of tissue factors in vitro [3]. The IBMIR is also reported in three different transplantations of allo-, auto-, and xenotransplantation for islets [5], as also caused by incompatible species between thrombotic factors of humans and regulatory molecules of pigs. IBMIR is explained to be not only a response occurred in transplantation of allogeneic and xenogeneic islets, but also a responsive phenomenon to the islets and the highly immunogenic cells surrounded with acinar tissues [5]. However, such hurdles are now resolved by α1,3Gal-T KO animals and transgenic gene manipulation of human genes of CD46/CD55/CD59 complement regulators [6]. Using the genetic engineering technology in the immunological-challenged baboon model, HR- and IBMIR-based phenomena have been prevented by the transgenic islets of pigs. Like the HR, IBMIR can be mitigated by genetically disrupting the α1,3Gal-T gene and by transducing human CD46, CD55, and CD59 complement regulators as transgenic genes, respectively, as the blood mediates inflammatory rejection and the regulators protect the inflammation.

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References

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Kim, CH. (2024). Blood-Mediated Inflammatory Reaction (IBMIR) and Prevention of IBMIR. In: Glycoimmunology in Xenotransplantation. Springer, Singapore. https://doi.org/10.1007/978-981-99-7691-1_13

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