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  • Title: Activation of glomerular basement membrane-specific B cells in the renal draining lymph node after T cell-mediated glomerular injury.
    Author: Robertson J, Wu J, Arends J, Zhou C, McMahon J, Torres L, Lou YH.
    Journal: J Am Soc Nephrol; 2005 Nov; 16(11):3256-63. PubMed ID: 16162812.
    Abstract:
    Linear binding of IgG to the glomerular basement membrane (GBM) is the hallmark of anti-GBM glomerulonephritis (GN). However, the precise mechanism by which diverse autoantibodies to GBM are induced in GN has not been determined. It was demonstrated previously that a single T cell epitope pCol(28-40) derived from collagen IV alpha3 chain not only induced severe GN in Wistar Kyoto rats but also triggered a diversified anti-GBM antibody response through "B cell epitope spreading." In this study, an expansion of T and B cells in the renal draining lymph node (RDLN) of diseased animals after glomerular injury was observed. RDLN was demonstrated to be the location of GBM-specific B cell activation. First, B cells from RDLN of pCol(28-40)-immunized rats produced in vitro anti-GBM antibodies and antinuclear antibodies. Second, B cells specific to the peptidic B cell epitope in pCol(28-40) were absent among expanding B cells in RDLN. Those findings provided a unique opportunity to track activation of diverse GBM-specific B cells in RDLN. Expression of B lymphocyte-induced maturation protein-1, which is involved in differentiation of plasma cells, in B cells of RDLN was detected and further elevated only after T cell-mediated prominent glomerular injury (day 19). This was supported by the fact that anti-GBM antibodies became detectable only after day 20. Those results suggest that T cell-mediated glomerular injury may trigger de novo internal immunization of autoantigens released from damaged GBM, which further leads to activation of a group of GBM-specific B cells in RDLN.
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