| First Author | Mannering SI | Year | 2000 |
| Journal | Immunology | Volume | 101 |
| Issue | 1 | Pages | 132-9 |
| PubMed ID | 11012764 | Mgi Jnum | J:110448 |
| Mgi Id | MGI:3640242 | Doi | 10.1046/j.1365-2567.2000.00075.x |
| Citation | Mannering SI, et al. (2000) T lymphocytes from granulocyte colony-stimulating factor-/- mice produce large quantities of interferon-gamma in a chronic infection model. Immunology 101(1):132-9 |
| abstractText | Little is known about the role of granulocyte colony-stimulating factor (G-CSF) in the response to chronic bacterial infections. To address this we infected G-CSF knock out (G-CSF-/-) mice with Mycobacterium avium. Infection was not exacerbated in G-CSF-/- mice despite a deficiency in the total bone marrow cells, colony-forming haemopoietic cells, granulocytes and monocyte precursors in the bone marrow. Peritoneal cells from G-CSF-/- produced less nitric oxide (NO) upon culture in vitro with antigen than did wild-type (WT) cells. Unexpectedly, T cells from infected G-CSF-/- mice were able to produce significantly more interferon-gamma (IFN-gamma) than the wild type (WT) controls. T cells from G-CSF-/- mice still produced more IFN-gamma even when in vitro NO production was inhibited, while enzyme-linked immunospot assay (ELISPOT) assays showed more IFN-gamma-producing cells in the G-CSF-/- mice. This was confirmed by intracellular cytokine staining (ICCS), which showed that there were more IFN-gamma producing T cells in vivo in the G-CSF-/- than the WT controls following M. avium infection. It is possible that a deficit of NO in vivo allows T cells to develop a higher IFN-gamma-producing phenotype. Thus we show a novel relationship between G-CSF and IFN-gamma production by T cells revealed in this chronic bacterial infection model. |
