Cancer vaccines are generally cancer treatment vaccines used to treat cancers that have already developed. The goal is to delay or stop cancer cell growth; to cause tumor shrinkage; to prevent cancer from coming back; or to eliminate cancer cells that have not been killed by other forms of treatment.

Cancer vaccines used for treatment are designed to work by activating cytotoxic T cells and directing them to recognize and attack specific types of cancer or by inducing the production of antibodies that bind to molecules on the surface of cancer cells. In order to achieve this, treatment vaccines introduce one or more antigens into the body, usually by injection, where they cause an immune response that results in T cell activation or antibody production. Antibodies recognize and bind to antigens on the surface of cancer cells, whereas T cells can also detect cancer antigens inside cancer cells.

To be effective, the cancer vaccines must achieve two goals: First, they must stimulate specific immune responses against the correct target. Second, the immune responses must be powerful enough to overcome the barriers that cancer cells use to protect themselves from attack by killer T cells.

Our department uses dendritic cells (DC) as vehicles for the vaccine antigen. These cells are called professional antigen presenting cells (APC) and are specialized in inducing potent T-cell responses.



Invariant Chain as a cancer vaccine (PI: S. Wälchli/O. Bakke at UiO):

Invariant chain (li) has traditionally been associated with antigen presentation on MHC class II to CD4+ T cells. Recently, however, we and others have demonstrated that li can also be involved in presentation to CD8+ T cells through MHC class I. Furthermore, we demonstrated that, by replacing the MHC binding part of li (CLIP) with an antigenic peptide, an immune response to the given target could be induced and thus serve as a potential vaccine (Wälchli et al. 2014).

Some questions still remain: in our article only the exact Class-I antigenic peptides were validated, and we had no evidence that Class I loading allowed flexibility: can we replace CLIP by a long peptide and still observe Class I loading? In addition, it was not know if combining overlapping peptide for Class I and Class II could evoke an immune response: Will a long peptide lead to competing fragment advantaging one of the MHC for loading?



Awards: CIMT 2012

Funding from Helse Sør-Øst Innovation grant

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