Animal Molecular Breeding 2024, Vol.14, No.1, 106-118 http://animalscipublisher.com/index.php/amb 108 Figure 1 EVs interact with cells via numerous ligand–receptor interactions (Adopted from Ravichandran et al., 2022) Image caption: sEVs can activate not only direct and indirect pathways of antigen presentation but also via the semidirect pathway in which T cell activation occurs via donor-derived sEVs (Adopted from Ravichandran et al., 2022) Ravichandran et al. (2022) shows the role of small extracellular vesicles (sEVs) in transplant rejection. sEVs, enriched with markers like CD9, CD63, and CD81, carry biomolecules specific to lung, heart, and kidney tissues. Lung sEVs with collagen type V and K alpha 1 tubulin indicate lung transplant rejection. Heart sEVs with myosin and vimentin and kidney sEVs with fibronectin and collagen IV are linked to heart and kidney transplant rejection, respectively. Monitoring these sEVs can provide early diagnostic markers for transplant rejection and aid in managing transplant patients. 2.2 Key genetic factors involved in immune rejection Genetic differences between donor and recipient, particularly in the MHC or human leukocyte antigen (HLA) genes, are the primary cause of immune rejection. Variations in these genes lead to the recognition of the transplanted organ as foreign by the recipient's immune system (Morazán-Fernández et al., 2022). Specific genes and their associated pathways have been identified as critical in the rejection process. For instance, the expression of interferon-gamma (IFNG)-inducible genes such as CXCL11 and IDO1, and genes associated with effector T cells and NK cells like KLRD1 and CCL4, are strongly linked to rejection (Halloran et al., 2018). Additionally, genes involved in the inflammasome pathway, such as AIM2, have been implicated in acute rejection, highlighting their potential as therapeutic targets (Tejada et al., 2022). Other important genetic factors include polymorphisms in cytokine genes like IL6, which have been associated with varying risks of acute rejection (Hu et al., 2024). 2.3 Mechanisms of hyperacute, acute, and chronic rejection Rejection of transplanted organs can occur at different stages, each with distinct mechanisms: Hyperacute Rejection: This occurs within minutes to hours after transplantation and is primarily mediated by pre-existing antibodies in the recipient that recognize antigens on the donor organ. These antibodies activate the complement system, leading to rapid and severe damage to the graft (Morazán-Fernández et al., 2022).
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