Emerging role of B cells in chronic allograft dysfunction Robert B. Colvin, Tsutomu Hirohashi, Alton B. Farris, Francesca Minnei, A. Bernard Collins, R. Neal Smith  Kidney International  Volume 78, Pages S13-S17 (December 2010) DOI: 10.1038/ki.2010.436 Copyright © 2010 International Society of Nephrology Terms and Conditions

Figure 1 Chronic antibody-mediated rejection. (a) Light microscopy of a case of transplant glomerulopathy shows a glomerulus with widespread duplication of the glomerular basement membrane (GBM) evident on periodic acid-Schiff stain (black arrows). Mononuclear cells are present in glomerular capillaries (glomerulitis) indicated with white arrows. (b) Prominent staining of peritubular capillaries for C4d is evident in a cryostat section of the same case. (c) Electron microscopy of another case shows reactive endothelial cells (E) that have lost their fenestrations and multilamination of the GBM (arrows). The original basement membrane is at the point of the arrows, the inner layers are newly formed. (d) Peritubular capillaries show similar multilamination (arrows) and loss of fenestrations. Kidney International 2010 78, S13-S17DOI: (10.1038/ki.2010.436) Copyright © 2010 International Society of Nephrology Terms and Conditions

Figure 2 Mouse heart allografts after adoptive transfer of class I donor-specific alloantibody into C3-/- RAG1-/- recipients, sampled at 28 days. (a) Marked intimal thickening in the proximal coronary artery (arrows) just distal to the aorta. (b) Lesions in the cellular phase (endarteritis) contain natural killer cells, which are indicated by arrows in this immunohistochemical stain with antibodies to Ly49g2 (ref. 36). Kidney International 2010 78, S13-S17DOI: (10.1038/ki.2010.436) Copyright © 2010 International Society of Nephrology Terms and Conditions