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A cytokine that seems to be heavily involved in tumour immunosuppression is the transforming growth factor beta (TGF-β), a protein that affects proliferation, activation, and differentiation of immune cells and inhibits antitumor immune response. In cancer cells, the production of TGF-β is increased and, in turn, raises their proteolytic activity and binding to cell adhesion molecules in the extracellular matrix. TGF-β can also convert effector T cells into Tregs. It has been reported that it can also promote angiogenesis and that this process can be blocked by anti-TGF-β antibodies.
Indeed, the mechanisms by which the tumour can evade immune system control are manifold. , 2007). Jeannin P et al. , 2011) reported that ovarian cancer ascites switched monocyte differentiation into tumour-associated macrophages (TAM)-like cells, that exhibit most phenotypic and functional characteristics of TAMs, suggesting that soluble mediators are involved in the differentiation of monocytes into TAM-like cells. TAMs, the most abundant immunosuppressive myeloid cells in the tumour microenvironment, exhibit an IL-10 (high) and IL-12 (low) profile called M2, opposite to the immunostimulatory M1.
Blocking antibodies against IL-6R inhibited both IL-6 production and EGF- and IL-6-induced migration. Specific inhibition of STAT3 activation by a JAK2-specific inhibitor blocked STAT3 phosphorylation, cell motility, induction of N-cadherin and vimentin expression and IL6 production. These data suggest that the activated status of STAT3 in high-grade EOC may occur directly through activation of 24 Ovarian Cancer – Basic Science Perspective EGFR or IL-6R or indirectly through induction of IL-6R signalling.