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Blood, Vol. 94 No. 3 (August 1), 1999:
pp. 1028-1037
Nitric Oxide Mediation of Active Immunosuppression Associated With
Graft-Versus-Host Reaction
Pierre Bobé,
Karim Benihoud,
Danièle Grandjon,
Paule Opolon,
Linda Louise Pritchard, and
Roger Huchet
From INSERM Unité 267 "Immunogénétique des
Allogreffes", Hôpital Paul Brousse, Villejuif Cedex, France;
Université Paris XI, Orsay Cedex, France; Service de Pathologie
Expérimentale, Institut Gustave Roussy, Villejuif Cedex, France;
and CNRS UPR 9079, IFR1221, Villejuif Cedex, France.
In the immunosuppression accompanying the lethal systemic
graft-versus-host reaction (GVHR) directed against minor
histocompatibility antigens in irradiated adult mice, we previously
determined that non-T, non-B, L-leucine methyl ester (LME)-sensitive
cells were implicated via two different mechanisms: one, which is
interferon- (IFN-)-dependent and affects both T-cell
proliferative responses and thymus-independent antibody production by
CD5+ B cells; and a second, which is IFN--independent
and affects B-cell proliferative responses. Because IFN- induces the
production of nitric oxide (NO), a potent
immunosuppressive molecule, we investigated the involvement of NO in
the suppression mediated by the LME-sensitive cells. Inducible NO
synthase (iNOS) mRNA, iNOS protein, and the stable end products of iNOS
pathway, L-citrulline and nitrite, were detected early in GVHR in
LME-sensitive spleen cells taken ex vivo and could be amplified in
vitro by T and B mitogens. Inhibition of NO production with arginine
analogs (aminoguanidine, NG-monomethyl-L-arginine
[LMMA]), like anti-IFN- antibodies, reversed suppression of both
T-cell responses to concanavalin A and CD5+ B-cell
responses, but not of B-cell response to lipopolysaccharides (LPS). The
GVHR-associated, IFN--dependent immunosuppression of T-cell
proliferation and of antibody synthesis by CD5+ B cells
is the consequence of NO production by LME-sensitive cells.
Immunohistochemical analyses indicate that these cells belong to the
macrophage lineage.
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