T lymphocytes from granulocyte colony-stimulating factor-/- mice produce large quantities of interferon-gamma in a chronic infection model.
AuthorMannering, SI; Zhan, Y; Gilbertson, B; Lieschke, GJ; Cheers, C
University of Melbourne Author/sGilbertson, Bradley
AffiliationMicrobiology & Immunology
MetadataShow full item record
Document TypeJournal Article
CitationMannering, SI; Zhan, Y; Gilbertson, B; Lieschke, GJ; Cheers, C, T lymphocytes from granulocyte colony-stimulating factor-/- mice produce large quantities of interferon-gamma in a chronic infection model., Immunology, 2000, 101 (1), pp. 132 - 139
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Open Access at PMChttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2327063
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.
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