Increased Complement Gene Expression in Circulating B Cells From Kidney Transplant Recipients With Chronic Antibody-Mediated Rejection

Chronic antibody-mediated rejection (CAMR) is a major cause of kidney allograft failure, commonly triggered by preformed or de novo antihuman leukocyte antigen donor-specific antibodies. After binding to graft endothelium, donor-specific antibodies activate the complement cascade that promotes graft injury.1 Intriguingly, animal data suggest that complement is implicated not only in the final donor-specific antibody effector mechanisms, but also in germinal center B cell maturation2 and antibody production.3 Whether complement affects donorspecific antibody production in human kidney transplant recipients is unknown. Herein, we assessed the strength of the association of 2 key complement-related genes, C1QA and C1QB, previously identified as differentially expressed in circulating leukocytes from 10 CAMR and 8 matched control kidney transplant recipients (Supplementary Table S1),4 with B cells, CD4þ T cells, CD8þ T cells, dendritic cells, monocytes, and natural killer cells.