Respiratory infections place a significant burden on global health. Understanding the inflammatory response to infections, such as influenza and Mycobacterium tuberculosis (Mtb), may assist the development of more effective vaccines or treatments. T-cell responses are critical for protection from these pathogens, and chemokine receptors play an important role in the recruitment of T-cells to the lungs. Previous studies have suggested links between CXCR6+ CD8+ T-cells in the lungs and protection against Mtb (Lee et al., Infect Immun., 2011). However the requirement for CXCR6 during pulmonary infection has not been elucidated. Utilising CXCR6-/- mice, the role of this receptor on vaccine-induced CD4+ T-cell responses was examined using a recombinant influenza A virus expressing the Mtb p25 peptide (rIAV-p25), that induces protection against Mtb (Flórido et al., EJI, 2015). Interestingly, CXCR6-/- mice lost less weight and recovered earlier after rIAV-p25 infection than wild type controls. There was no defect in the recruitment of T-cells to the lungs after rIAV-p25, but there was a reduction in Th1-cytokine production. Further, in an aerosol model of Mtb infection, we demonstrated that CXCR6 was redundant for the early recruitment of T-cells. Interestingly, at 6 weeks post-infection, CXCR6-/- mice showed reduced bacterial counts in the lungs and decreased local Th1-cytokine production. Therefore, while CXCR6 deficiency has minimal impact on T-cell recruitment to the lungs, it may modulate inflammatory kinetics in mice with influenza or Mtb, and this may be beneficial to the clearance of pathogens. An appreciation for the role of chemokine receptors in pulmonary inflammation may aid the future development of preventative strategies.