Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1910629 | Free Radical Biology and Medicine | 2009 | 7 Pages |
Abstract
Spleens of mice injected with heat-killed Mycobacterium tuberculosis increase their Gr-1+ cell content and develop a system of interactive Ly-6G+ and Ly-6GâGr-1+ populations or “Greg” subsets, which, upon stimulation by activated T cells, produce immunoregulatory superoxide (O2â) and nitric oxide (NO), respectively. The balance between immunosuppressive NO and its antagonist O2â regulates T cell expansion, similar to regulation of vasodilation. Reduction of NO levels by O2â is required for efficient T cell expansion and development of autoimmunity. We studied the source of Gr-1+ cells in bone marrow (BM), where their levels were higher than in spleen, with both Greg subsets expressing strong activity. In the spleens of primed IL-23â/â mice, Ly-6G+ cells remained at naïve levels and produced no O2â. The complementary Ly-6GâGr-1+ splenocytes and their suppressive activity were partially reduced. Surprisingly, Gr-1+ cell levels in BM of IL-23â/â mice were increased, as were their O2â and NO production. Transfer of primed BM cells partially restored regulatory function in the spleen of IL-23â/â recipients. The results suggest that IL-23 is involved in mobilization of O2â- and NO-producing Gr-1+ cells from BM, which may contribute to its widely studied role in (auto)immunity.
Keywords
mAbFITCCFASFUl-NMAEAEAPCiNOScomplete Freund's adjuvantmonoclonal AbN-monométhyl-L-arginineNBT, Nitroblue tetrazoliumallophycocyaninexperimental autoimmune encephalitisFree radicalsSODImmunosuppressionMyeloid cellsinducible nitric oxide synthaseSuperoxideSuperoxide dismutasegranulocyte colony-stimulating factorG-CSFfluorescein isothiocyanateMycobacterium tuberculosisbone marrowwild typeNitric oxideAntibody
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Authors
Therese A. Dietlin, Daniel J. Cua, Kathleen A. Burke, Brett T. Lund, Roel C. van der Veen,