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  • Title: Transfection of L929 cells with complement subcomponent C1q B-chain antisense cDNA inhibits tumor necrosis factor-alpha binding to mediate cytotoxicity and nitric oxide generation.
    Author: Jiang H, Stewart CA, Tan SY, Fast DJ, Rummage JA, Leu RW.
    Journal: Cell Immunol; 1996 Feb 01; 167(2):293-301. PubMed ID: 8603439.
    Abstract:
    The role of complement subcomponent C1q in the modulation of TNF-alpha 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-alpha 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-alpha 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-alpha, IFN-alpha/beta, and LPS. Taken together, these results indicate that endogenously synthesized C1q is prerequisite for binding of TNF-alpha to L929 cells to mediate cytotoxicity and NO generation.
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