Abstract
An effective cancer vaccine should stimulate cytotoxic T cells (CTL), helper T cells and antibodies. The CTLs will efficiently kill all tumour cells expressing target antigen and class I MHC. Helper T cells responding to MHC class II presented epitopes will help in the production of CTLs but will also migrate to tissues expressing locally presented target antigen. Once they have localised within the tissues they will release the cytotoxic cytokines (TNFα, INFβ, IFNγ) and recruit non specific effector cells such as macrophages; there is also evidence that the products of CD4 T cells can damage the vasculature of tumours[1]. All of these effects will result in tumour cell death of antigen positive or negative cells. They are therefore synergistic with CTL killing. T helper cells can also recruit natural killer (NK) cells that will kill any tumour cells that have lost MHC expression[2]. As this is a common mechanism for tumours to evade CTL killing it is an important component of any immune response induced by a cancer vaccine. The potential of antibody responses to contribute to anti-tumour effects is less clear. The ‘type 1’ T cells that help in the activation of CTLs can help in the production of specific subclasses of antibodies (IgG2a in mice and IgG1in humans). These antibodies will kill any tumour cell expressing target antigen by antibody dependent cellular cytotoxicity that is mediated by Fc receptor expressing leucocytes, including NK cells. T helper cell recruitment of NK cells into tumour tissues is therefore also essential for antibody mediated tumour killing. Complement fixation could also play a role, either as a lytic effector mechanism, or as a trigger for activating local immune responses. The remainder of this chapter will now consider how an anti-idiotypic antibody can fulfil these requirements for this effective cancer vaccine.
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Durrant, L.G., Spendlove, I., Robins, R.A. (2001). Anti-idiotypic vaccination. In: Robins, R.A., Rees, R.C. (eds) Cancer Immunology. Immunology and Medicine Series, vol 30. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-0963-7_10
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DOI: https://doi.org/10.1007/978-94-017-0963-7_10
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