Extended Data Fig. 5: The schematic model of the role of LILRB3 in inflammation and ferroptosis.
From: LILRB3 genetic variation is associated with kidney transplant failure in African American recipients
Activation of LILRB3 causes binding and activation of SHP1/2 phosphatases that, through crosstalk, limit inflammatory signals initiated by TLR stimuli (for example, LPS) among other stimuli. The expression of the variant LILRB3-4SNPs risk allele reduces the capability of LILRB3’s intracellular ITIM domain to bind to and activate SHP1/2 phosphatases, resulting in amplification of the inflammatory response (for example, TNFα and cytokine release) and JAK/STAT activation, facilitate induction of ferroptosis, ultimately leading to graft damages. Figure created with BioRender.com.
