Down-regulation of HLA antigens by the adenovirus type 2 E3/19K protein in a T-lymphoma cell line.

摘要: Adenoviruses of subgroup C can establish persistent infections in human beings. The exact site persistence has not been established, but lymphoid tissues are certainly one reservoir. Experimental evidence suggests that early transcription unit 3 (E3) the virus is involved this phenomenon. In particular, most abundant protein region, E3/19K protein, seems to fulfill an important role viral escape from immune response. We previously demonstrated nonlymphoid cells interferes with antigen presentation function class I major histocompatibility complex (MHC) antigens by inhibiting their transport cell surface. However, E3 products was investigated. To examine this, T-lymphoma line Jurkat transfected a DNA fragment comprising entire region adenovirus type 2. show here expressed absence transactivator E1A rate biosynthesis similar 293 cells. Furthermore, inhibition and down-regulation MHC comparable both lines. contrast, various T-cell molecules containing immunoglobulin-like domains showed normal expression pattern A detailed analysis interaction between (HLA-A3 HLA-B35) revealed differential sensitivity for E3/19K. data demonstrate exerts its also without affecting other surface molecules. implications vivo discussed.