| First Author | Dietlin TA | Year | 2009 |
| Journal | Free Radic Biol Med | Volume | 47 |
| Issue | 4 | Pages | 357-63 |
| PubMed ID | 19409487 | Mgi Jnum | J:151191 |
| Mgi Id | MGI:4352981 | Doi | 10.1016/j.freeradbiomed.2009.04.029 |
| Citation | Dietlin TA, et al. (2009) Role of IL-23 in mobilization of immunoregulatory nitric oxide- or superoxide-producing Gr-1+ cells from bone marrow. Free Radic Biol Med 47(4):357-63 |
| abstractText | 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-6G-Gr-1+ populations or 'Greg' subsets, which, upon stimulation by activated T cells, produce immunoregulatory superoxide (O2(-)) and nitric oxide (NO), respectively. The balance between immunosuppressive NO and its antagonist O2(-) regulates T cell expansion, similar to regulation of vasodilation. Reduction of NO levels by O2(-) 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-23-/- mice, Ly-6G+ cells remained at naive levels and produced no O2(-). The complementary Ly-6G(-)Gr-1+ splenocytes and their suppressive activity were partially reduced. Surprisingly, Gr-1+ cell levels in BM of IL-23-/- mice were increased, as were their O2(-) and NO production. Transfer of primed BM cells partially restored regulatory function in the spleen of IL-23-/- recipients. The results suggest that IL-23 is involved in mobilization of O2(-)- and NO-producing Gr-1+ cells from BM, which may contribute to its widely studied role in (auto)immunity. |
