Defective formation of IgA memory B cells, Th1 and Th17 cells in symptomatic patients with selective IgA deficiency.
Christina Grosserichter-WagenerAlexander Franco-GallegoFatemeh AhmadiMarcela Moncada-VélezVirgil Ash DalmJessica Lineth RojasJulio César OrregoNatalia Correa VargasLennart HammarströmMarco Wj SchreursWillem A DikP Martin van HagenLouis BoonJacques Jm van DongenMirjam van der BurgQiang Pan-HammarströmJose Luis FrancoMenno C van ZelmPublished in: Clinical & translational immunology (2020)
Impaired IgA memory formation in sIgAD patients is not due to a B-cell activation defect. Instead, decreased Th1 and Th17 cell numbers and high blood levels of BAFF, APRIL and TGF-β1 might reflect disturbed regulation of IgA responses in vivo.These insights into B-cell extrinsic immune defects suggest the need for a broader immunological focus on genomics and functional analyses to unravel the pathogenesis of sIgAD.