The effect of CD4+ T cell response makes IL‐6 crucial in the protection against murine M. tuberculosis infection. IL‐6 deficiency resulted in an altered Th1 response and raised bacterial loads. M. tuberculosis‐infected macrophages secreted IL‐6 which overturned the responses of uninfected macrophages to interferon (IFN). Elevated IL‐6 in the lungs and increased concentrations of IL‐1β correlated with TB progression. IL‐6 was shown to positively and negatively contribute to host control against TB infection. This evidence concerns the gene IFNA1 and tuberculosis.