| Autor: |
Jiang, Hong, Stewart, Charles A., Tan, Shi-yu, Fast, David J., Rummage, John A., Leu, Richard W. |
| Zdroj: |
Cellular Immunology; February 1996, Vol. 167 Issue: 2 p293-301, 9p |
| Abstrakt: |
The role of complement subcomponent C1q in the modulation of TNF-α binding to L929 cells to mediate cytotoxicity and nitric oxide (NO) generation was investigated. Transfection of L929 with murine C1q B-chain antisense plasmid cDNA rendered them markedly less susceptible to TNF-mediated cytotoxicity coincident with a decreased capacity for TNF-α binding and expression of cell surface C1q protein. The inhibitory effects of L929 transfection with C1q B-chain antisense were transiently expressed at 24 hr post-transfection with full recovery of cellular functions by 72 hr. Transfected L929 cells were fully reconstituted in their TNF-α binding and in their cytotoxic response following exposure to soluble C1q which was bound to their cell surface. Transfection with C1q B-chain antisense also significantly inhibited NO generation by L929 cells in response to stimulation by TNF-α, IFN-α/β, and LPS. Taken together, these results indicate that endogenously synthesized C1q is prerequisite for binding of TNF-α to L929 cells to mediate cytotoxicity and NO generation. |
| Databáze: |
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