Increased T cell cytotoxicity by Betathine-induced upregulation of TNFalpha.

Article Details

Citation
Copy to clipboard

Dunn TM, Wormsley S, Taub FE, Pontzer CH

Increased T cell cytotoxicity by Betathine-induced upregulation of TNFalpha.

Int J Immunopharmacol. 2000 Mar;22(3):213-27.

PubMed ID
10685004 [ View in PubMed
]
Abstract

Betathine (BT) is a low molecular weight disulfide that has previously been shown to exhibit in vivo antitumor activity in murine myeloma and melanoma models. We have shown that BT treatment of both human T cells and monocytes is associated with an increase in surface tumor necrosis alpha (TNFalpha) expression. Further, in T cells and monocytes that have been stimulated with PMA and ionomycin, the addition of BT results in a dose and time dependent increase in the percentage of high TNFalpha-expressing cells. Unlike TNFalpha upregulation produced by the commonly used thiol antioxidant N-acetyl-L-cysteine (NAC), the BT-induced increase in TNFalpha is observed consistently in different donors. This increase in surface TNFalpha is associated with elevated levels of TNFalpha mRNA. In addition, expression of TNFalpha receptor I is also significantly enhanced by BT treatment. The upregulation of surface TNFalpha by BT has functional consequences, in that, BT-treated T cells exhibit enhanced cytotoxic activity. Thus, increased TNFalpha expression may be one mechanism responsible for the antineoplastic activity of BT.

DrugBank Data that Cites this Article

Drugs