1. Figure 2 Emerging models of antibody-mediated rejection (ABMR) and
T cell-mediated rejection (TCMR) mechanisms
Figure 2 | Emerging models of antibody-mediated rejection (ABMR) and T cell-mediated rejection (TCMR) mechanisms. a | In ABMR, natural killer (NK) cells bind to the endothelium by CD16a (also known as FcγRIII)-mediated recognition of the Fc region of endothelium-bound anti-donor antibodies. Activation of CD16a Fc receptors triggers the release of IFNγ and antibody-dependent NK-cell-mediated cytotoxicity. Additional interaction between NK cells and the endothelium might occur via complement receptors expressed by NK cells. b | In TCMR, effector T cells penetrate the endothelium and interact with antigen presenting cells and macrophages. Activation of T cell receptors (TCRs) activates an inflammatory response dependent on events triggered by the synapse between effector T cells and antigen-presenting cells (for example, IFNγ release). The expression of inhibitory checkpoints (such as interactions between CTLA4 and CD80 and between PD1 (also known as PDCD1) and PD1 ligands such as CD274 (also known as PDCD1LG1)) raises the possibility of the negative control of T cells by antigen presenting cells. Selected genes that are highly associated with the molecular landscape of ABMR and TCMR are shown. ADCC, antibody-dependent cellular cytotoxicity; AKI, acute kidney injury; MHC, major histocompatibility complex.
Halloran, P. F. et al. (2016) Molecular assessment of disease states in kidney transplant biopsy samples
Nat. Rev. Nephrol. doi: /nrneph