Furthermore, Harding and colleagues have shown, in vivo, that an extended OVA peptide, noncovalently associated with mycobacterial HSP70, could be presented via the MHC I presentation pathways of bone-marrow-derived murine macrophages and DCs to induce the secretion of IL-2 from a T-cell hybridoma specific for OVA peptide/MHC I complex [ 78].
Certain DC subsets appear to be specialized to take up non-infectious antigenic materials, process and present such antigens along the MHC class I presentation pathway to naïve CD8+ T cells via 'cross-presentation' [36], [37], [38].
The chaperoned peptides can be channelled into the endogenous class I presentation pathway of a subset of professional antigen-presenting cells, which are then able to prime CD8-positive CTLs.
Rapid pMHC I presentation apparently occurs because infected cells can synthesize and present peptides from antigenic precursors called defective ribosomal products (DRiPs).
The pathway leading to MHC class I presentation begins when proteins are degraded by the proteasome, which is present in the cytosol.
Therefore, alternative vaccine delivery systems, which enable introduction of nonreplicating antigen into the MHC class I presentation pathway, are sought.
The influence of aligned, collagen type I (Col I) presentation in IPC hydrogel on chondrogenic differentiation of human mesenchymal stem cells (MSC) was investigated.
Three signals are required for T-cell activation: (i) presentation of cognate antigen in self MHC molecules; (ii) costimulation by membrane-bound receptor-ligand pairs; and (iii) soluble factors to direct polarization of the ensuing immune response.
To conclude, we showed that Salmonella can be designed to deliver antigen(s) to the host cell cytosol for presumably class I presentation for the induction of protective immune responses.
Yet, recent evidence suggests that autophagy stimulates MHC class I presentation [43].
The GAr could affect pMHC I presentation by inhibiting proteolytic activity of the proteasome [26], [27].
