Therefore, we hypothesized that there exists an imbalance of Th1/Th17 in cavitary PTB: IL-17 might participate in the formation of pulmonary cavities in tuberculosis; immune protection might decrease while immune pathology increases in cavitary tuberculosis; and Th1/Th17 in cavitary PTB might be lower than in non-cavitary PTB. Here, IL17A is linked to tuberculosis.