T-cell receptor recognizing M72-derived peptide–MHC complex (TCR-M72-pMHC)

T-cell receptors (TCRs) recognizing M72-derived peptide–MHC complexes are critical components of the adaptive immune response against Mycobacterium tuberculosis (Van Der Meeren et al., 2018, NEJM). The M72 antigen is a recombinant fusion protein comprising two immunogenic mycobacterial proteins, Mtb32A (Rv0125) and Mtb39A (Rv1196), designed to elicit a robust T-cell response (Penn-Nicholson et al., 2015, Vaccine). When these antigens are processed and presented as peptides on Major Histocompatibility Complex (MHC) molecules, specific TCRs bind to them, triggering T-cell activation. This interaction is the primary mechanism by which the M72/AS01E vaccine candidate induces protective immunity, primarily through the generation of polyfunctional CD4+ T-cells (Tait et al., 2019, NEJM). These activated T-cells produce essential cytokines such as interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), which are vital for macrophage activation and the containment of the pathogen (Gillard et al., 2016, Expert Review of Vaccines). Understanding the diversity and specificity of these TCRs is essential for evaluating vaccine efficacy and the longevity of the immune memory. Consequently, these receptors serve as the functional target for vaccine-induced cellular immunity in the prevention of pulmonary tuberculosis.

Other names

M72-specific T-cell receptorTCR recognizing Mtb32A/Mtb39A peptidesMycobacterium tuberculosis-specific T-cell receptorM72-specific TCR

Recognition of M72-derived peptides presented by MHC molecules, leading to the activation of antigen-specific T-cells and the subsequent release of pro-inflammatory cytokines like IFN-gamma and TNF-alpha to control Mycobacterium tuberculosis infection (Van Der Meeren et al., 2018).