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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]