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Blood, Vol. 95 No. 1 (January 1), 2000:
pp. 212-220
Nitric oxide-producing
CD11b+Ly-6G(Gr-1)+CD31(ER-MP12)+
cells in the spleen of cyclophosphamide-treated mice:
implications for T-cell responses in immunosuppressed mice
Iñigo Angulo,
Federico Gómez de las Heras,
José F. García-Bustos,
Domingo Gargallo,
M. Angeles Muñoz-Fernández, and
Manuel Fresno
From the Centro de Biología Molecular, CSIC-Universidad
Autónoma de Madrid, Spain; GlaxoWellcome S.A., Tres Cantos,
Spain; and the Department of Immunology, Hospital Gregorio
Marañón, Madrid, Spain.
During recovery from intensive chemotherapy with cyclophosphamide
(CTX), mice suffer a severe but transitory impairment in spleen cell
proliferation to T-cell mitogens (Con A or anti-CD3 plus IL-2).
Although CTX treatment reduced spleen T-cell cellularity, this cannot
fully account for T-cell unresponsiveness. The results showed that CTX
induces the colonization of spleen by an immature myeloid
CD11b+Ly-6G+CD31+ population.
Its presence closely correlated with the maximum inhibition of T-cell
proliferation. Moreover, this suppressive activity was dependent on
nitric oxide (NO) production in cultures since (1) higher amounts of
nitric oxide and inducible nitric oxide synthase (iNOS) mRNA were
produced in CTX spleen cells (CTX-SC) than in control splenocyte
cultures and (2) NOS inhibitors greatly improved the proliferation of T
lymphocytes. Nitric oxide production and suppressive activity were also
dependent on endogenous interferon- (IFN-) production since
anti-IFN- abrogated both effects. Finally, iNOS protein expression
was restricted to a heterogeneous population of CD31+
cells in which CD11b+Ly-6G+ cells were
required to suppress T-cell proliferation. These results indicated that
CTX might also cause immunosuppression by a mechanism involving the
presence of immature myeloid cells with suppressor activity. This may
have implications in clinical praxis since inappropriate
immunotherapies in patients treated with intensive chemotherapy could
lead to deleterious T-cell responses. (Blood. 2000;95:212-220)
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