The first evidence of cross-presentation was reported in 1976 by Michael J. Bevan after injection of grafted cells carrying foreign minor histocompatibility (MiHA) molecules.
All mDCs have specialized functions and secretory factors, but they are all still able to cross present antigens in order to activate cytotoxic CD8+ T cells.
[11] In addition to solid structure uptake, dendritic cell phagocytosis simultaneously modifies the kinetics of endosomal trafficking and maturation.
[6] Endocytosis results in the formation of a phagocytic vesicle, where an increasingly acidic environment along with the activation of enzymes such as lysosomal proteases triggers the degradation of antigen into peptides.
There is also evidence that suggest that cross-presentation requires a separate pathway in a proportion of CD8(+) dendritic cells that are able to cross-present.
[10] After antigen peptide loading, the MHC molecule is transported out of the ER, through the Golgi complex, and then onto the cell surface for cross presentation.
[10] It appears that both pathways are able to occur within an antigen presenting cell, and may be influenced by environmental factors such as proteasome and phagocytic inhibitors.
[6] Cross-presentation has been shown to play a role in the immune defense against many viruses (herpesvirus, influenzavirus, CMV, EBV, SIV, papillomavirus, and others), bacteria (listeria, salmonella, E. coli, M. tuberculosis, and others) and tumors (brain, pancreas, melanoma, leukemia, and others).
[17] The action of cross priming can bolster immunity against antigens that target intracellular peripheral tissues that are unable to be mediated by antibodies produced through B cells.
Overall, cross presentation aids in facilitating an adaptive immune response against intracellular viruses and tumor cells.
[6] Cross-presenting DCs are able to induce anergy, apoptosis, or T regulatory states for high self affinity T cytotoxic cells.
This has large implications for defense against auto immune disorders and regulation of self specific cytotoxic T cells.