The effect of Chlamydophila pneumoniae Major Outer Membrane Protein (MOMP) on macrophage and T cell-mediated immune responses

A Novel Transport Mechanism for MOMP in Chlamydophila pneumoniae and Its Putative Role in Immune-Therapy

“…Such suboptimal binding topologies have been reported myelin basic protein/HLA-DR4 complex as a mechanism for escape from negative selection [66], iii) induction of an overwhelming protective signal by the resulting MHC-peptide complex, iv) stimulation of the generation of suppressive/regulatory T cell clones that dampens down inflammation through the synthesis and secretion of anti-inflammatory cytokines such as IL-10 and TGF beta [12] and, v) competitive binding of anti-inflammatory MOMP-derived peptides. Such a mechanism is supported by experiments, showing the effect of a single amino acid change in collagen II-derived peptide on loss of T cell activation, demonstrated by [67].…”

“…Murine and human MHC alleles were selected for computational analysis in this study, since I-Ab represents an already experimentally determined case study in the C57Bl/6J apoE−/− mice model [12]. Furthermore, I-Ab is bound to a CLIP peptide, which is a conserved step in the posttranslational processing of MHC proteins.…”

“…It has been suggested that Chlamydophila pneumoniae potentiates inflammation/development of atherosclerosis by at least one of the following mechanisms; induction of matrix metalloproteinases [8], induction of macrophages to secrete adhesion molecules, cytokines [9], [10], enhancing oxidative remodelling of low density lipoprotein [9] and calcification of atherosclerotic plaques [11]. We have recently suggested another mechanism which involves the dampening of anti-Chlamydophila antibody and T cell responses [12].…”

“…Preliminary evidence suggests that the purified MOMP of Chlamydophila pneumoniae has anti-atherosclerotic and anti-inflammatory effects [12], [19]–[21]. This mechanism could potentially favour Chlamydophila’s survival within macrophages while keeping a slow chronic induction of inflammation within atherosclerotic plaques contributing to their development over many years.…”

Predicting protein transport mechanism and immune response using spatial protein motifs and epitopes

“…MOMP from Chlamydophila pneumoniae and Chlamydia trachomatis, the human pathogens, to date, remain the best characterised. In addition, MOMP-derived peptides have been shown to potentiate anti-inflammatory and anti-atherogenecity, by a cell mediated system involving MHC class II proteins [2]. However, despite the importance of this protein as a vaccine target against inflammation driven pathologies attributed to Chlamydia, tremendous challenges in the isolation of this membrane-bound, cysteine-rich protein make it difficult to experimentally isolate the protein for detailed structural and immunological studies.…”