T-cell receptor recognizing Chlamydia trachomatis Major Outer Membrane Protein (MOMP) peptides (TCR-MOMP)

T-cell receptors (TCRs) that recognize peptides derived from the Major Outer Membrane Protein (MOMP) of Chlamydia trachomatis, when presented by MHC class II molecules, are the primary mediators of protective cellular immunity against chlamydial infections (Poston et al., 2019, Journal of Immunology). MOMP is a porin-like protein that is highly conserved across various serovars and contains multiple CD4+ T-cell epitopes, making it a focal point for vaccine development (UniProt P0CL43). Upon binding to the MOMP peptide-MHC II complex on antigen-presenting cells, these TCRs trigger the activation of CD4+ T cells, which subsequently differentiate into Th1 and Th17 effector cells (Olsen et al., 2021, The Lancet Infectious Diseases). These effector cells produce critical cytokines such as interferon-gamma (IFN-γ) and interleukin-17 (IL-17), which are necessary for the recruitment of phagocytes and the ultimate clearance of the intracellular pathogen (Finco et al., 2011, Vaccine). Therapeutic strategies, particularly recombinant vaccines like CTH522, aim to prime and expand this specific TCR repertoire to provide long-lasting immunity against genital tract infections and ocular trachoma (Olsen et al., 2021). However, the high degree of MHC polymorphism in human populations and the potential for immunopathology remain significant challenges in targeting these receptors effectively (Poston et al., 2019).

Other names

MOMP-specific T-cell receptorChlamydia-specific CD4+ TCRMOMP-MHC II complex receptorMajor Outer Membrane Protein-specific T-cell receptor

Activation of CD4+ T-helper cells through the recognition of MOMP-derived epitopes presented by MHC class II molecules, leading to a Th1-mediated immune response and pathogen clearance.