Transforming growth factor-β2 down-regulates HLA-DR antigen expression on human malignant glioma cells.
✍ Scribed by Patrick Zuber; Maria C. Kuppner; Nicolas De Tribolet
- Publisher
- John Wiley and Sons
- Year
- 1988
- Tongue
- English
- Weight
- 531 KB
- Volume
- 18
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Transforming growth factor-fi2 down-regulates HLA-DR antigen expression on human malignant glioma cells
Transforming growth factor-fl (TGF-P) is known to have a potent inhibitory influence on several immune functions. It has recently been demonstrated that TGF-P2 is identical to the glioblastoma-derived T cell suppressor factor (G-TsF). In the present study, human malignant glioma cell lines were incubated with various concentrations of TGF-P2. An optimal concentration of 1 ng/ml TGF-P2 produced a partial but significant decrease of HLA-DR (class 11) surface antigen expression on glioma cells expressing this antigen, as well as decreased levels of HLA-DR-specific mRNA. The surface expression of other HLA-related molecules, such as HLA-ABC (class I) and Pz-microglobulin, was not influenced by TGF-P2. The suppressive effect of TGF-P2 on HLA-DR expression, both at the surface antigenic and cytoplasmic mRNA levels, could be completely overcome by adding relatively high concentrations (500 U/ml) of interferon (1FN)-y to the culture system. However, TGF-62 inhibited the enhancement of HLA-DR surface expression produced by low concentrations of IFN-y on some cells which initially did not express these antigens. These results show that TGF-p2 can act as a regulator of HLA-DR antigen expression on human glioma cells.
📜 SIMILAR VOLUMES
The relationship between the expression of selected oncogenes having different modes of action and the loss of the capacity t o respond in vitro to transforming growth factor+ I (TGF-P I) was analyzed in human mammary epithelial cells (MEC). Primary MEC cultures from healthy donors and the spontaneo
## Abstract The net balance between urokinase‐type plasminogen activator (uPA) and plasminogen activator inhibitor type‐1 (PAI‐1) has been implicated in tumor cell invasion and metastasis. To elucidate the mechanism of the transforming growth factor‐β1 (TGF‐β1)‐dependent up‐regulation of PAI‐1 expr