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Sensitized CD4+ and CD8+ T-lymphocytes are specialized immune cells that mediate the adaptive immune response against mycobacterial species, most notably Mycobacterium tuberculosis (Jasenosky et al., 2015). These cells are primed during initial infection or vaccination, where they learn to recognize specific mycobacterial peptides presented by Major Histocompatibility Complex (MHC) molecules on the surface of antigen-presenting cells (Lewinsohn et al., 2011). CD4+ T cells primarily recognize MHC Class II complexes and orchestrate the immune response by secreting pro-inflammatory cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) to activate macrophages (Cooper, 2009). CD8+ T cells recognize MHC Class I complexes and exert direct cytotoxic effects on infected cells through the release of perforin, granzymes, and granulysin (Flynn & Chan, 2001). This T-cell-mediated immunity is the cornerstone of host defense, as it is required for the formation and maintenance of granulomas that sequester the pathogen (Kaufmann, 2010). In clinical practice, these cells are the focus of diagnostic Interferon-Gamma Release Assays (IGRAs) which measure the T-cell response to specific TB antigens (Pai et al., 2014). Furthermore, these sensitized T cells are the primary biological target for the development of novel tuberculosis vaccines, which aim to enhance their frequency and protective efficacy (Kaufmann, 2010).
Recognition of mycobacterial antigens via the T-cell receptor (TCR) leads to cellular activation, cytokine secretion, and direct cytotoxicity against infected cells (Jasenosky et al., 2015; Lewinsohn et al., 2011).
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