Abstract
Greater understanding of the immunopathogenesis of tuberculosis is critical for developing novel therapies. Here, we propose that immunothrombosis plays an important role in the immune response to Mycobacterium tuberculosis. This interplay among macrophages, neutrophils, and platelets leads to microthrombosis at the site of infection, trapping the mycobacterium to prevent dissemination. We explore how dysregulated immunothrombosis might contribute to tuberculosis pathogenesis, with excessive microthrombosis driving drug resistance, leading to lung damage and venous thromboembolism. Further research into these poorly understood mechanisms could identify options for host-directed therapies to ameliorate immunothrombosis, with its attendant tissue destruction, and reduce the burden of resistance.