Innate immune response to tumour cells
Cancer cells can alter the steady state activity of all myeloid cells
present in the tumour microenvironment by secreting IL-6 or
granulocyte-macrophage colony-stimulating factor ( GM-CSF), that induce
the recruitment of immature myeloid cells to tumour cells, as well as
cell proliferation. Natural killer cells (NKL) can kill target cells
without the need for prior activation. As many neoplastic cells lose the
expression of MHC-I during malignant transformation which at normal
levels inhibit NK cells, they continue to express ligands (e.g.
glycolipid) that activate NK cells. This recognition mechanism further
leads to the progression of anti- tumour immune response through the
production of interferon-λ which activate a number of interferon- λ
signalling pathways that enhances the killing of a proportion of the
tumour, induces the production of chemokines that further recruits more
cells in the innate immune system, activates macrophages that express
tumoricidal products (reactive oxygen and nitrogen metabolites) and,
tumour necrosis factor(TNF) that activates endothelial cells and
coagulation leading to tumour necrosis, and directly stimulates
apoptosis. Moreover, the cytokines, IL-12. IL-15, and the type 1
interferons stimulate NK cells, which leads to proliferation and
increased cytotoxic activity [32].