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Suppression of B-cell proliferation to lipopolysaccharide is mediated
through induction of the nitric oxide pathway by tumor necrosis factor-
alpha in mice with acute graft-versus-host disease
G Falzarano, W Krenger, KM Snyder, J Delmonte , M Karandikar and JL Ferrara
Division of Pediatric Oncology, Dana-Farber Cancer Institute and Children's
Hospital, Boston, MA, USA.
Graft-versus-host disease (GVHD) is associated with impaired B-cell
responses. We investigated the mechanism of impaired proliferation of B
cells in response to the mitogen lipopolysaccharide (LPS) by analyzing the
production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide
(NO), both of which have independently been described as important effector
mechanisms in the pathogenesis of acute GVHD. A threefold decrease of
mature surface Ig-positive (slg+) B cells was observed in GVHD spleens
isolated 2 weeks after transplant. However, proliferation of these cells in
response to LPS was suppressed by more than 35-fold. Activated GVHD
splenocytes secreted large amounts of TNF- alpha and NO in culture.
Neutralization of TNF-alpha with anti-TNF- alpha antibody (Ab) both
abrogated NO production and restored LPS- induced proliferation of B cells
to levels found in non-GVHD control mice. The specific inhibition of NO
synthesis with LG-monomethyl- arginine (NMMA) restored splenocyte responses
but did not significantly reduce TNF-alpha levels, showing that TNF-alpha
per se did not cause immunosuppression. These data show that, during GVHD,
induction of the NO pathway is an important mechanism that mediates B-cell
hyporesponsiveness to LPS and that this pathway is induced by TNF-alpha.
Volume 87,
Issue 7,
pp. 2853-2860,
04/01/1996
Copyright © 1996 by The American Society of Hematology
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