Tuberculosis is a global public health catastrophe responsible for >8 million cases of illness and 2 million deaths annually. Pulmonary cavitation with cough-generated aerosol is the principle means of spread, and lung remodeling (healed cavitation, fibrosis, and bronchiectasis) is a major cause of lung disability, surpassing all other diffuse parenchymal lung diseases combined. Efficient granuloma turnover is mycobactericidal, and extracellular matrix is disbanded without scarring. In many with progressive disease, however, there is dysregulated granuloma turnover, liquefactive necrosis, and pathological scarring. The pathological mechanisms and the related immunological pathways underpinning these phenomena are reviewed in the present article. Further studies are needed to identify and develop specific immunotherapeutic interventions that target immunopathology, since they have the potential to substantially reduce spread.