Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the world¹ and our current understanding of the biology underpinning this disease is poor. Polymorphisms and mutations in haematopoietic cell kinase (Hck) have been observed in patients with COPD and lung cancer while aberrant activation of Hck promotes inflammatory disease and airspace enlargement in the lungs of mice similar to COPD in humans². To investigate the role of Hck in pulmonary inflammation and cancer in mice, we used genetic complementation to investigate the contribution of the immune systems to inflammation in Hck mutant mice that harbour a constitutive active kinase (Hck^Up/Up). Adult Hck^Up/Up mice develop pulmonary inflammation as indicated by an increased macrophage, neutrophil and eosinophil numbers in BAL fluid compared to Wt mice, which progressed to emphysema from 12 weeks of age. A contribution of the adaptive immune system to disease was discounted since lymphocyte (Hck^Up/Up;Rag1^-/-) and Th₂-deficient (Hck^Up/Up;Stat6^-/-) mice retained abundant macrophages in bronchoalveolar lavage fluid (BALF). Mutant macrophages were implicated in promoting disease after adoptive transfer of Wt bone marrow alleviated disease in Hck^Up/Up host mice and haploinsufficiency for Csf1r (Hck^Up/Up;Csfr1^+/-) culminated in reduced macrophage numbers in the BALF. Genetic depletion of TNF-α or MyD88 also partially rescued the inflammation phenotype of Hck^Up/Up mice, while IL-6 was causally linked to disease after no inflammation was observed in Hck^Up/Up;Il6^-/- mice. We detected a striking bias towards expression of genes associated with alternatively activated macrophages in BALF cells and bone marrow-derived macrophages of Hck^Up/Up mice. Surprisingly, Hck-dependent polarisation of alveolar macrophages, but not of interstitial macrophages, was associated with COPD-like disease. Furthermore, lung tumour burden was significantly larger in Hck^Up/Up;Kras^LSL-G12D/+ mice than in Kras^LSL-G12D/+, consistent with alternative macrophage polarisation promoting cancer progression and COPD as an independent risk factor for lung cancer development. Hck activity within alveolar macrophages promotes alternative macrophage polarisation to drive a COPD-like inflammatory pulmonary disease and lung tumour progression in mice.