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Table 2 Tumor immune evasion mechanisms and DV infection

From: Overcoming tumor immune evasion with an unique arbovirus

Immune evasion Dengue counter-attack
Low levels of MHC on tumor cell prevent CTL recognition [11] Hi Interferon-γ raises MHC levels by up-regulating MHC gene expression [37,52]
Point mutations in Tumor Peptides prevent TCR binding [12] LAK/CIK cells target “escaped” tumor cells expressing aberrant peptides or MHC [40,56]
Tumor vessels lack factors for CTL attachment and trafficking [12] Hi [TNF-a] restores gaps by altering PECAM-1, restores ICAM-1/VCAM-1 expression and P and E-selectins [22,57]
FasL can kill Fas+ CTL by triggering apoptosis [12] Hi [IL-6, 15] protects Fas+ CTL by up-regulating FLIP ligand [58,59]
HLA-G protects from NK Cells [12] Hi [IL-2,7,12,15 raise activation of NK [56,60]
Stromal barriers inhibit CTL [12] Hi [IFN-γ] activates Macrophages to M1 [36]
Myeloid-Derived Suppressor Cells, (MDSC) [61] iNKT Cells can decrease MDSC [61]
CTL inactivated by TGF-β [12] TH1 cytokines reactivate tolerant CTL [51,62]
Tumor PI-9 blocks CTL killing ([63] Hi [CD8] & ICAM-1 expression can restore low-avidity CTL recognition and lysis by stabilizing weak interactions between TCR and MHC + self-peptide [64]
T-regulatory cells block CTL [61] Hi CD4Helper cells overcome CD4Reg cells [37,61]