Reprogramming the tumor microenvironment: tumor-induced immunosuppressive factors paralyze T cells

The regulatory role of B cells in autoimmunity, infections and cancer: Perspectives beyond IL10 production

“…Like in PD-L1 + Tregs which can transduce an inhibitory signal into effector T cells through interacting with programmed death-1 (PD-1), PD-L1-expressing B cells also have been proved to exert a suppressive role on PD1-expressing CD8 + T cells, inhibiting their proliferation and effector functions in Salmonella infection [34] and cancer [35]. Considering the great impact of PD-1/PD-L1 pathway on cancer and viral infection progression [36][37][38], more studies about PD-L1-expressing B cells or their products of differentiation are needed.…”

STAT3 inhibition for cancer therapy: Cell-autonomous effects only?

“…4 Indeed, the inhibition of STAT3 in cancer cells is expected to limit the production of pro-inflammatory factors (such as IL-6), hence reducing local inflammatory reactions that may contribute to tumor progression. 4,[10][11][12] Moreover, the inhibition of STAT3 allows malignant cells to secrete high amounts of Type I interferon and other products of so-called interferon response genes (IRGs), including chemokine (C-X-C motif) ligand 9 (CXCL9) and CXCL10. 13,14 By virtue of this mechanism, STAT3 inhibition stimulates the recruitment of immune effectors into the tumor bed and improves immunosurveillance, especially in the context of ongoing anticancer immune responses.…”

Colorectal Cancer Immunotherapy: Current State and Prospects (Review)

“…Typically, NKG2D are expressed only on the surface of senescent or malignized cells providing their elimination by the immune system [23]. However, due to the immunoediting, the expression of NKG2D ligands in a tumor is often suppressed [24]. Therefore, the recovery of the interaction so important for tumor elimination by introducing NKG2D ligand associated with the antibody against tumor antigen can be a promising therapeutic method.…”