An antigen-specific chimeric autoantibody receptor (CAAR) NK cell strategy for the elimination of anti-PLA2R1 and anti-THSD7A antibody-secreting cells
Larissa Seifert, Kristoffer Riecken, Gunther Zahner, Julia Hambach, Julia Hagenstein, Gudrun Dubberke, Tobias B. Huber, Friedrich Koch‐Nolte, Boris Fehse, Nicola M. Tomas
Abstract
Membranous nephropathy (MN) is an antibody-mediated disease of the kidney, typically resulting in nephrotic syndrome with urinary loss of high amounts of albumin and other plasma proteins. Phospholipase A2 receptor 1 (PLA2R1) and thrombospondin type-1 domain-containing protein 7A (THSD7A) were the first renal autoantigens identified in adult patients with MN.1,2 Importantly, we and others could demonstrate that autoantibodies in MN are not only excellent biomarkers to monitor immunological disease activity, but also cause the disease through the direct interaction with the autoantigen expressed on podocytes in the kidney.