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and Nitric Oxide-Dependent Mechanism
*
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115; and
Neose Technologies, Horsham, PA 19044
Lacto-N-fucopentaose III (LNFPIII) is found in human
milk and on the Th2 driving helminth parasite Schistosoma
mansoni. This pentasaccharide drives Th2-type responses in vivo
and in vitro when conjugated to a carrier. In an attempt to further
understand early events in Th1 to Th2 switching, we examined phenotypic
and functional changes in peritoneal cell populations in BALB/c and
SCID mice following LNFPIII-dextran injection. We found that i.p.
injection with LNFPIII-dextran resulted in rapid (<20 h) expansion of
the Gr1+ subpopulation of
F4/80+/CD11b+ peritoneal cells, comprising up
to 75% of F4/80+/CD11b+ peritoneal cells
compared with 18% in uninjected or dextran-injected mice.
Functionally, these cells suppressed anti-CD3- and
anti-CD28-induced proliferation of naive CD4+ T cells.
LNFPIII-dextran also expanded functional Gr1+ suppressor
macrophages in SCID mice, demonstrating that expansion and function of
suppressor cells did not require T cells. Suppression in both BALB/c
and SCID mice was NO and IFN-
dependent, as addition of inhibitors
of inducible NO synthase
(NG-monomethyl-L-arginine), as
well as anti-IFN- Abs, restored the ability of CD4+
T cells to proliferate in vitro. Depletion of the F4/80+
subset of Gr1+ cells eliminated the suppressive activity of
peritoneal exudate cells showing that these cells were macrophages.
Thus, LNFPIII-dextran rapidly expands the Gr1+ suppressor
macrophage population in the peritoneal cavities of otherwise naive
mice. These Gr1+ cells suppress proliferation of naive
CD4+ T cells in an NO-dependent mechanism, and may play a
regulatory role in the switching of Th1- to Th2-type
responses.
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