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The "Host immune system via expressed Mycobacterium tuberculosis antigens" refers to the spectrum of human immune mechanisms—innate and adaptive—triggered by recognition of antigens (proteins, peptides, lipid components) expressed by *Mycobacterium tuberculosis* during infection. Key immune components include macrophages, dendritic cells, and T lymphocytes, which interact with Mtb antigens through various pattern recognition receptors (such as Toll-like receptors, C-type lectins, and MHC molecules), leading to the activation of immune responses, including cytokine secretion (e.g., IFN-γ, TNF-α), T cell priming, and antibody production. Mtb has evolved sophisticated strategies to evade and modulate these responses, such as inhibiting antigen presentation, dampening proinflammatory signaling, and altering host cell death pathways, complicating both natural defense and vaccine design. Major immunodominant antigens (e.g., Ag85 complex, ESAT-6, TB10.4) are the focus of diagnostics and vaccine research. This entry describes a host-pathogen interaction and immune process, not a canonical druggable target. For structured target information, it is necessary to specify either a particular *Mycobacterium tuberculosis* antigen (e.g., ESAT-6, Ag85B) or a specific component of the host immune system (e.g., TLR2, DC-SIGN, MHC II) involved in Mtb recognition and response.
Induction of adaptive and innate immune responses through recognition of Mtb antigens (by vaccines or adjuvants) leading to T cell activation and cytokine release; Enhancement of antigen presentation or modulation of host immunity
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