Mycobacterium tuberculosis antigens presented by Major Histocompatibility Complex (Mtb-pMHC)

Mycobacterium tuberculosis (Mtb) antigens presented by the Major Histocompatibility Complex (MHC) are the primary targets for cellular immune recognition during tuberculosis infection. These targets are not individual proteins in the traditional sense but are peptide fragments derived from Mtb proteins—such as ESAT-6, CFP-10, and the Antigen 85 complex—that are processed and displayed on the surface of infected macrophages via MHC Class I and Class II molecules (Flynn & Chan, 2001; Sorensen et al., 1995). The recognition of these peptide-MHC (pMHC) complexes by T-cell receptors (TCRs) is fundamental to the host's ability to mount a protective immune response, involving the secretion of pro-inflammatory cytokines like interferon-gamma (IFN-γ) and the direct lysis of infected cells (Jasenosky et al., 2015). In clinical practice, these immunological targets are exploited for both diagnostics and vaccine development. Vaccines like BCG and newer candidates such as M72/AS01E aim to prime the immune system to recognize these specific antigens more effectively upon exposure to Mtb (Tait et al., 2019). However, the high degree of polymorphism in human HLA genes and the ability of Mtb to evade immune detection by modulating antigen presentation present significant therapeutic challenges. Furthermore, excessive immune activation against these targets can lead to tissue damage or the Koch phenomenon, a severe inflammatory response in individuals with pre-existing sensitivity to Mtb antigens (Andersen, 2007).

Other names

Mycobacterium tuberculosis antigensMtb T-cell epitopesMtb peptide-MHC complexesMtb pMHCTuberculosis antigens

Induction of antigen-specific T-cell mediated immunity through the recognition of Mycobacterium tuberculosis-derived peptides (e.g., ESAT-6, CFP-10, Ag85B) presented on host MHC Class I and Class II molecules by T-cell receptors (TCRs), leading to cytokine production and macrophage activation (Flynn & Chan, 2001; Jasenosky et al., 2015).