Renal localization of the membrane attack complex in systemic lupus erythematosus nephritis

doi:10.1084/jem.154.6.1779

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Renal localization of the membrane attack complex in systemic lupus erythematosus nephritis

G Biesecker, S Katz and D Koffler

The membrane attack complex (MAC) of the complement system was localized in both glomeruli and peritubular regions of 22 kidneys manifesting systemic lupus erythematosus (SLE) nephritis. A similar distribution was observed for immune complex markers (IgG, Clq, and C3) and MAC in glomeruli, although the deposits of MAC were more discrete and showed lesser immunofluorescence staining intensity compared with immunoglobulins and complement components. In contrast, peritubular immune complexes were present in only 7 out of 22 kidneys, involved comparatively small clusters of tubules, exhibited weaker immunofluorescence staining than MAC, and failed to correlate with interstitial foci of inflammation. Granular or irregular, linear aggregates of the MAC were observed at the periphery of larger groups of tubules contiguous to areas of interstitial inflammation. Comparable amounts of IgG, Clq, C3, and MAC were present in blood vessel walls in areas of fibrinoid necrosis. These data suggest that the MAC is a direct mediator of tissue injury occurring in renal glomeruli, tubules, and blood vessels. The discordance between immune complexes and MAC localized in the peritubular region, but not in glomeruli or blood vessels, raises the possibility that both immune complexes and nonimmune agents, such as bacterial antigens, may activate the classical or alternative complement pathways and thereby play a role in the pathogenesis of tubulointerstitial lesions of SLE nephritis.
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Lidington, E. A., Haskard, D. O., Mason, J. C. (2000). Induction of decay-accelerating factor by thrombin through a protease-activated receptor 1 and protein kinase C-dependent pathway protects vascular endothelial cells from complement-mediated injury. Blood 96: 2784-2792 [Abstract] [Full Text]
NANGAKU, M., PIPPIN, J., COUSER, W. G. (1999). Complement Membrane Attack Complex (C5b-9) Mediates Interstitial Disease in Experimental Nephrotic Syndrome. J. Am. Soc. Nephrol. 10: 2323-2331 [Abstract] [Full Text]
Tokumoto, M., Fukuda, K., Shinozaki, M., Kashiwagi, M., Katafuchi, R., Yoshida, T., Yanagida, T., Kanai, H., Hirakata, H., Tamaki, K., Okuda, S., Fujishima, M. (1999). Acute interstitial nephritis with immune complex deposition and MHC class II antigen presentation along the tubular basement membrane. Nephrol Dial Transplant 14: 2210-2215 [Full Text]
Mason, J. C., Yarwood, H., Sugars, K., Morgan, B. P., Davies, K. A., Haskard, D. O. (1999). Induction of Decay-Accelerating Factor by Cytokines or the Membrane-Attack Complex Protects Vascular Endothelial Cells Against Complement Deposition. Blood 94: 1673-1682 [Abstract] [Full Text]
Hindmarsh, E. J., Marks, R. M. (1998). Complement Activation Occurs on Subendothelial Extracellular Matrix In Vitro and Is Initiated by Retraction or Removal of Overlying Endothelial Cells. J. Immunol. 160: 6128-6136 [Abstract] [Full Text]
Eichenfield, L. F., Johnston, R. B. Jr (1989). Secondary Disorders of the Complement System. Arch Pediatr Adolesc Med 143: 595-602 [Abstract]