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3 Chain Noncollagen Domain 1 Is Not Associated with Glomerular Basement Membrane Antibody: A Potential T Cell-Mediated Mechanism1
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Department of Basic Sciences, Dental Branch, University of Texas Houston Health Science Center, Houston, TX 77030;
Department of Pathology, Texas Children’s Hospital, Baylor College of Medicine, Houston, TX 77030; and
Department of Pathology, University of Virginia, Charlottesville, VA 22908
Glomerulonephritis is believed to result commonly from Ab-mediated
glomerular injury. However, Ab-associated mechanisms alone cannot
explain many cases of human glomerulonephritis. We developed a rat
model of human anti-glomerular basement membrane (GBM) disease to
investigate T cell and Ab response, and their associations with the
disease. A single immunization of highly denatured recombinant mouse
collagen IV
3 chain noncollagen domain 1 (rCol43NC1) induced
severe glomerulonephritis in 100% of Wistar Kyoto rats, 33% of which
died of this disease around day 35 postimmunization. The renal
pathology demonstrated widespread glomerular damage and a mononuclear
cell infiltration within the interstitial tissue. T cells from
immunized rats responded not only to rCol43NC1, but also to isolated
rat GBM. Sera Abs to rCol43NC1 were detectable in 100% of the rats,
but only 20% of the rats had low levels of Ab to isolated rat GBM by
Western blot, and none by immunofluorescence. Furthermore, IgG/M
binding to or C3 deposition on endogenous GBM in immunized rats were
not detected in most of the experimental rats, and showed no
statistical correlation with disease severity. Additionally, no
electronic dense deposition in the glomeruli was detected in all rats.
Those data revealed a disassociation between the disease and
anti-GBM Ab. T cell-mediated mechanisms, which are currently under
our investigation, may be responsible for the glomerular
disease.
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