Glioma stem cells (GSCs) decrease T cells cognition and evade systemic immunosurveillance via downregulations or defects of major histocompatibility complex class I (MHC-I) molecule and antigen-processing machinery (APM) components.
No human major histocompatibility complex class 1 (MHC-I) was detected in the resistant glioma line, while infection of the susceptible glioma cell lines, which expressed human MHC-I, were blocked with antibody to MHC-I, indicating that human MHC-I acts as an EHV-1 entry receptor on glioma cells.
Human alloreactive CTL interactions with gliomas and with those having upregulated HLA expression from exogenous IFN-gamma or IFN-gamma gene modification.
Thus, HLA-DRB1*15:DRB5*(51) occurrence in combination with HLA-DRB1*11 was associated with a 13.4-fold increased risk of glioma (p = 0.001), and the incidence of HLA-Cw*6:DRB1*07 with a 0.2-fold decreased risk of glioma (p = 0.03).
Recently, using the IGF-I triple helix approach in studies of tumorigenicity, major histocompatibility complex class I (MHC-I) antigens were demonstrated in rat glioma transfected cells.
This increased expression of MHC-I and B-7, demonstrated by 51Cr release complement dependent cytoxicity assay and by immunostaining flow cytometry analysis, could contribute to the final immune recognition of glioma immunogenicity.