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J Leukoc Biol. 2007 May;81(5):1205-12. Epub 2007 Feb 16.

Mycobacteria-induced Gr-1+ subsets from distinct myeloid lineages have opposite effects on T cell expansion.

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Department of Neurology, University of Southern California Keck School of Medicine, MCA 245, 1333 San Pablo Street, Los Angeles, CA 90033, USA.


Similar to the regulation of vasodilation, the balance between NO and superoxide (O2-) regulates expansion of activated T cells in mice. Reduction of suppressive NO levels by O2- is essential for T cell expansion and development of autoimmunity. In mice primed with heat-killed Mycobacterium, a splenocyte population positive for Gr-1 (Ly-6G/C) is the exclusive source of both immunoregulatory free radicals. Distinct Gr-1+ cell subpopulations were separated according to Ly-6G expression. In culture with activated T cells, predominantly monocytic Ly-6G- Gr-1+ cells produced T cell-inhibitory NO but no O2-. However, mostly granulocytic Ly-6G+ cells produced O2- simultaneously but had no measurable effect on proliferation. Recombination of the two purified Gr-1+ subpopulations restored controlled regulation of T cell proliferation through NO and O2- interaction. Coculture of p47phox-/- and inducible NO synthase-/- Gr-1+ cells confirmed this intercellular interaction. These data suggest that bacterial products induce development of distinct Gr-1+ myeloid lineages, which upon stimulation by activated T cells, interact via their respective free radical products to modulate T cell expansion.

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