This review examines the immune mechanisms underlying granuloma formation in sarcoidosis and tuberculosis (TB), comparing the processes in these two diseases. Sarcoidosis is a complex immune-mediated disease characterized by the formation of granulomas, which are clusters of immune cells. The review highlights the role of *Mycobacterium tuberculosis* in initiating granuloma formation in TB, while in sarcoidosis, the granuloma is driven by diverse genetic variants and antigens. Key immune cells involved in granuloma formation include macrophages, lymphocytes, monocytes, neutrophils, and T cells. Macrophages, particularly CD4+ T lymphocytes, are crucial in both diseases, but the mechanisms of their activation and function differ. In TB, macrophages recognize *M. tuberculosis* antigens and trigger a coordinated immune response, while in sarcoidosis, the immune response is driven by genetic factors and diverse antigens. The review also discusses the role of mTORC1 signaling, which is activated in both diseases but for different reasons. In TB, mTORC1 activation is induced by the pathogen, while in sarcoidosis, it is likely due to mutations in genes involved in autophagy and intracellular vesicular transport. The review concludes with a comparison of granuloma composition and structure in TB and sarcoidosis, noting that TB granulomas are more immunosuppressive due to the presence of IDO1+ myeloid cells, while sarcoidosis granulomas are characterized by high levels of CD4+ T cells and metabolic shifts. Recent single-cell transcriptomic studies provide detailed insights into the immune landscape of granulomas, highlighting the importance of metabolically reprogrammed macrophages, active IFN-γ-producing CD4+ T cells, and Th171 cells in sarcoidosis. Overall, the review underscores the complex interplay between genetic factors, antigens, and immune cell dynamics in the development and maintenance of granulomas in these two diseases.This review examines the immune mechanisms underlying granuloma formation in sarcoidosis and tuberculosis (TB), comparing the processes in these two diseases. Sarcoidosis is a complex immune-mediated disease characterized by the formation of granulomas, which are clusters of immune cells. The review highlights the role of *Mycobacterium tuberculosis* in initiating granuloma formation in TB, while in sarcoidosis, the granuloma is driven by diverse genetic variants and antigens. Key immune cells involved in granuloma formation include macrophages, lymphocytes, monocytes, neutrophils, and T cells. Macrophages, particularly CD4+ T lymphocytes, are crucial in both diseases, but the mechanisms of their activation and function differ. In TB, macrophages recognize *M. tuberculosis* antigens and trigger a coordinated immune response, while in sarcoidosis, the immune response is driven by genetic factors and diverse antigens. The review also discusses the role of mTORC1 signaling, which is activated in both diseases but for different reasons. In TB, mTORC1 activation is induced by the pathogen, while in sarcoidosis, it is likely due to mutations in genes involved in autophagy and intracellular vesicular transport. The review concludes with a comparison of granuloma composition and structure in TB and sarcoidosis, noting that TB granulomas are more immunosuppressive due to the presence of IDO1+ myeloid cells, while sarcoidosis granulomas are characterized by high levels of CD4+ T cells and metabolic shifts. Recent single-cell transcriptomic studies provide detailed insights into the immune landscape of granulomas, highlighting the importance of metabolically reprogrammed macrophages, active IFN-γ-producing CD4+ T cells, and Th171 cells in sarcoidosis. Overall, the review underscores the complex interplay between genetic factors, antigens, and immune cell dynamics in the development and maintenance of granulomas in these two diseases.