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J. Exp. Med.,
Volume 188, Number 10, November 16, 1998 1775-1784
By
From the Department of Medicine, Liverpool Hospital and the University of New South Wales,
Liverpool, New South Wales 2170, Australia
Active Heymann nephritis (HN) is a rat model of human idiopathic membranous nephropathy
in which injury is thought to be mediated by membrane attack complex of complement
(MAC) activated by antibody (Ab) to glomerular epithelial cells. Recent work has shown that HN develops in C6-deficient rats which cannot assemble MAC, and that infiltration of activated cytotoxic CD8+ T cells and macrophages into glomeruli coincides with proteinuria. This
study examined the role of CD8+ T cells in mediating glomerular injury in HN by permanent
CD8+ cytotoxic T cell depletion via adult thymectomy (ATx) and anti-CD8 mAb. Groups of
rats were depleted of CD8+ T cells either before immunization for HN or 6 wk after immunization when Ab responses and glomerular IgG deposition were well established. These were
compared with groups of HN, ATx/HN, and complete Freund's adjuvant (CFA) controls.
Neither group of CD8+ T cell-depleted rats developed proteinuria, although there was normal
development and deposition of Ab. CD8+ T cell-depleted rats developed neither T cell or
macrophage infiltrates nor their effector cytokines, which are present in glomeruli of rats with
HN. Examination of lymph node (LN) draining sites of immunization showed these findings
were not explained by altered immune events within these LNs. It was concluded that CD8+
cytotoxic T cells are essential to the mediation of glomerular injury in HN and may be relevant
to the pathogenesis and treatment of membranous nephropathy.
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