Immune responses in pulmonary tuberculosis: A concise review

Pulmonary tuberculosis (PTB) caused by Mycobacterium tuberculosis (MTB), remains a major global health concern due to its high morbidity and mortality rates, especially in resource-limited settings. The pathophysiology of tuberculosis (TB) is characterized by complex interactions between the human host immune system and the pathogen. Alveolar macrophages are especially vulnerable targets of MTB, triggering a cascade of pro-inflammatory and anti-inflammatory responses that either contain the infection or facilitate progression to active disease. In addition, recent advances in immunopathology have highlighted the roles of cytokine networks, T-cell responses, and immune checkpoints in disease progression. A deeper understanding of TB pathophysiology has significant implications for clinical management and research. It aids in the development of novel diagnostic biomarkers, host-directed therapies, and more effective vaccine strategies. Emerging therapeutic approaches focus on modulating the immune response to enhance MTB clearance while minimizing tissue damage. Moreover, drug-resistant TB strains pose a growing challenge, necessitating research into host-pathogen interactions that could lead to more effective treatment strategies. This review provides a concise examination of the key mechanisms underlying PTB, emphasizing recent scientific advancements and their relevance for clinicians and researchers. By bridging the gap between basic science and clinical application, this work aims to contribute to the ongoing efforts to improve TB control and patient outcomes.