Monitor your body's response and report any unusual reactions
As such, the damage-associated molecular patterns (DAMPs) that are released in response to the ischemia during the graft preparation are recognized by pattern recognition receptors (PRRs) of phagocytic cells of the innate immunity leading to the upregulation of costimulatory molecules and secretion of pro-inflammatory cytokines ( Figure 1 ) and act in concert with innate immunity-derived stimuli to activate and expand recipient T cell clones with inflammatory or regulatory functions ( Fas ligand which is also known as tumor necrosis factor (TNF) ligand superfamily member 6, interferon (IFN)-, TNF, CXC-chemokine ligand (CXCL) 10, CC-chemokine ligand (CCL) 2, CCL3, CCL4, CCL5, and CX3CL1, potentiates the inflammatory injury that is the characteristics of acute allograft rejection ( Figure 1 Currently, the Banff classification ( i) interstitial inflammation in the non-scarred area of the cortex, ii) tubulitis in cortical tubules within the non-scarred cortex, and iii) endarteritis (intimal and transmural arteritis with fibrinoid necrotic change) as well as medial smooth muscle necrosis with lymphocytic infiltration in the vessel ( 2.2 Antibody-mediated rejection Antibody-mediated rejection (AMR) is the most severe and destructive form of immune-mediated graft injury which is observed in approximately 30% of all patients with rejection ( + T cells, which are activated by epitopes expressed on graft antigens, assist in the activation of graft-specific B cells, which is followed by class switching and affinity maturation
Radenkovic, D., Reason & Verdin, E
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