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  Indian J Med Microbiol
 

Figure 1. Role of mesenchymal stromal cells (MSC) in tumour microenvironment: priming with aminobisphosphonates can trigger anti-tumour immunity. MSC through different soluble factors as prostaglandin E2 (PGE2), indoleaminedioxigenase (IDO) and transforming growth factor (TGF)β can downregulate anti-tumour immune response triggered through NKG2D-NKG2DL interaction. In addition, TGFβ can stimulate epithelial mesenchymal transition (EMT) and further metastasization of tumour cells. The priming of MSC with aminobishosphonates (NBPs) induces an imbalance between the production of TGFβ and interleukin (IL)15. TGFβ is an immune regulating factor compared with the immunostimulation elicited with IL15. This leads to the triggering, rather than inhibition, of anti-tumour immune response with the consequent tumour cell killing. Cytolytic T lymphocytes (CTL) and γδ T cells are the main effector mediators of tumour cell elimination. Further, the reduction in TGFβ production can impair the EMT and the consequent metastasization of tumour cells.

Figure 1. Role of mesenchymal stromal cells (MSC) in tumour microenvironment: priming with aminobisphosphonates can trigger anti-tumour immunity. MSC through different soluble factors as prostaglandin E2 (PGE2), indoleaminedioxigenase (IDO) and transforming growth factor (TGF)β can downregulate anti-tumour immune response triggered through NKG2D-NKG2DL interaction. In addition, TGFβ can stimulate epithelial mesenchymal transition (EMT) and further metastasization of tumour cells. The priming of MSC with aminobishosphonates (NBPs) induces an imbalance between the production of TGFβ and interleukin (IL)15. TGFβ is an immune regulating factor compared with the immunostimulation elicited with IL15. This leads to the triggering, rather than inhibition, of anti-tumour immune response with the consequent tumour cell killing. Cytolytic T lymphocytes (CTL) and γδ T cells are the main effector mediators of tumour cell elimination. Further, the reduction in TGFβ production can impair the EMT and the consequent metastasization of tumour cells.