CD99 Regulates the Transport of MHC Class I Molecules from the Golgi Complex to the Cell Surface1
The results suggest that CD99 may be associated with the post-Golgi trafficking machinery by regulating the transport to the plasma membrane rather than the endocytosis of surface MHC class I molecules, providing a novel mechanism of M HC class I down-regulation for immune escape.
Suicide cancer gene therapy using pore-forming toxin, streptolysin O
The results show that the genes of pore-forming toxins, like streptolysin O protein, have the potential to establish a novel class of suicide gene therapeutic reagents.
DC-SIGN expression in Hofbauer cells may play an important role in immune tolerance in fetal chorionic villi during the development of preeclampsia.
Targeted cytotoxic effect of anti-JL1 immunotoxin against a human leukemic cell line and its clinical implications
Galonin-conjugated anti-JL1 mAb immunotoxin could be developed as a potential immunotherapeutic agent in the treatment of various types of JL1-positive acute leukemias.
MHC class II engagement inhibits CD99‐induced apoptosis and up‐regulation of T cell receptor and MHC molecules in human thymocytes and T cell line
Mutations of the immunoglobulin heavy chain variable region gene in CD99-deficient BJAB cell line.
It is reported that CD99 downregulated BJAB cell line has several mutations in IgH V genes, which might be the basis for the understanding of the molecular and cellular mechanism that regulate somatic mutation and B cell selection.
CD 99 expression is positively regulated by Sp 1 and is negatively regulated by Epstein-Barr virus latent membrane protein 1 through nuclear factor-k B
Data suggest that Sp1 activates, whereas LMP1 represses, transcription from the CD99 promoter through the NF-kB signaling pathway, and they might aid in the understanding of the molecular mechanisms of viral pathogenesis in EBVpositive Hodgkin disease.
Cell Surface I Molecules from the Golgi Complex to the CD99 Regulates the Transport of MHC Class
The results suggest that CD99 may be associated with the post-Golgi trafﬁcking machinery by regulating the transport to the plasma membrane rather than the endocytosis of surface MHC class I molecules, providing a novel mechanism of M HC class I downregulation for immune escape.