Host cell death and immune response modulation against Mycobacterium tuberculosis (Mtb) infection are critical for controlling tuberculosis (TB). Mtb, the causative agent of TB, is a major global health concern, with TB causing millions of deaths annually. The immune system, particularly the innate and adaptive responses, plays a key role in containing Mtb. Granulomas, formed by immune cells, are a hallmark of TB pathology, helping to wall off the pathogen. However, Mtb has evolved mechanisms to evade immune responses, leading to persistent infection. Host cell death, including apoptosis, autophagy, and necrosis, is a key mechanism in the immune response to Mtb. Apoptosis, a programmed cell death, helps contain Mtb by limiting its replication and facilitating the clearance of infected cells. Necrosis, on the other hand, benefits Mtb by allowing the release of bacteria into the environment. Mtb can also manipulate these pathways to enhance its survival and persistence. The immune system, particularly macrophages, plays a central role in the initial response to Mtb. Cytokines such as TNF-α and IFN-γ are crucial for activating macrophages and coordinating the immune response. Autophagy, a cellular process that degrades intracellular pathogens, is also important in controlling Mtb. However, Mtb can subvert autophagy to survive within host cells. The review discusses the diverse mechanisms underlying Mtb-induced host cell death and their implications for immune response modulation. It highlights the potential of targeting host cell death pathways as therapeutic strategies against TB. Therapeutic agents targeting autophagy, apoptosis, and necrosis are being investigated for their potential to enhance the immune response and control Mtb infection. The review also emphasizes the importance of understanding these pathways to develop effective treatments and vaccines for TB.Host cell death and immune response modulation against Mycobacterium tuberculosis (Mtb) infection are critical for controlling tuberculosis (TB). Mtb, the causative agent of TB, is a major global health concern, with TB causing millions of deaths annually. The immune system, particularly the innate and adaptive responses, plays a key role in containing Mtb. Granulomas, formed by immune cells, are a hallmark of TB pathology, helping to wall off the pathogen. However, Mtb has evolved mechanisms to evade immune responses, leading to persistent infection. Host cell death, including apoptosis, autophagy, and necrosis, is a key mechanism in the immune response to Mtb. Apoptosis, a programmed cell death, helps contain Mtb by limiting its replication and facilitating the clearance of infected cells. Necrosis, on the other hand, benefits Mtb by allowing the release of bacteria into the environment. Mtb can also manipulate these pathways to enhance its survival and persistence. The immune system, particularly macrophages, plays a central role in the initial response to Mtb. Cytokines such as TNF-α and IFN-γ are crucial for activating macrophages and coordinating the immune response. Autophagy, a cellular process that degrades intracellular pathogens, is also important in controlling Mtb. However, Mtb can subvert autophagy to survive within host cells. The review discusses the diverse mechanisms underlying Mtb-induced host cell death and their implications for immune response modulation. It highlights the potential of targeting host cell death pathways as therapeutic strategies against TB. Therapeutic agents targeting autophagy, apoptosis, and necrosis are being investigated for their potential to enhance the immune response and control Mtb infection. The review also emphasizes the importance of understanding these pathways to develop effective treatments and vaccines for TB.