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‐γ (IFN‐γ) than the wild type (WT) controls. T cells from G‐CSF^–/– mice still produced more IFN‐γ even when in vitro NO production was inhibited, while enzyme‐linked immunospot assay (ELISPOT) assays showed more IFN‐γ‐producing cells in the G‐CSF^–/– mice. This was confirmed by intracellular cytokine staining (ICCS), which showed that there were more IFN‐γ 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‐γ‐producing phenotype. Thus we show a novel relationship between G‐CSF and IFN‐γ production by T cells revealed in this chronic bacterial infection model.