Role of Th2 Cytokines in the Course of Tuberculosis Infection: Immunological Insights and Clinical Implications

Background: Tuberculosis (TB), caused by Mycobacterium-tuberculosis, is a major global infectious killer. The imbalance between Th1 and Th2 immune responses plays a key role in disease progression, tissue damage, and treatment outcomes. Th1 cells drive cell-mediated immunity, while Th2 cells promote humoral immunity. Th2 cytokines like IL-4 and IL-13 can worsen control of intracellular M. tuberculosis infection. Specifically, IL-4 can induce the development of regulatory T cells (CD25+ Tregs) from naive CD4+ T cells, which become anergic and suppress the proliferation of other T cells, similar to natural Tregs. This work aimed to assess the role of Th2 cytokines, specifically IL-4 and IL-10, in tuberculosis pathogenesis. It focused on how these cytokines contribute to disease progression, modulate the host immune response, and affect bacterial load. Study examined differences in cytokine impact on pulmonary versus extrapulmonary TB and explored how alternatively activated macrophages influence the immune environment during infection. A thorough literature search was performed using Scopus, PubMed, Web of Science, and Google Scholar. Included studies addressed TB immunopathogenesis, clinical presentation, diagnostic approaches, and management, with particular emphasis on Th2 cytokine activity. The collected evidence was organized into thematic areas encompassing epidemiology, etiology, host immune response, clinical features, diagnostics, and therapeutic strategies. Conclusion: TB continues to pose a major worldwide health burden, where the immune balance determines disease outcome. Th2 cytokines, particularly IL-4 and-10, had a dual function: moderating inflammation but also weakening protective Th1 responses, allowing bacillary persistence and contributing to fibrosis and cavitation