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Biomedical subjects

C C Ting

Publications and source records attributed to C C Ting.

89 records · Page 5Linked to original sources

Expression of fetal antigens in tumor cells.

The activities of sera that reacted specifically with the specific cell-surface antigens of polyoma or simian virus 40 tumors could only be inhibited by absorption of the sera with tumor cells transformed by the specific virus, and could not be removed by the absorption with cells from various fetal tissues nor with cells from other tumors. In contrasts, the antisera produced in male C3H/HeN mice by inoculation of irradiated, syngeneic fetal tissue of 1- to 2-weeks gestation, reacted with various tumor cells. The activities of these sera, when tested against cells from tumors induced by polyoma virus or simian virus 40, could also be removed by absorption with cells from tumors induced by viruses other than polyoma or simian virus 40, including leukemia cells induced by Gross virus (C58NT)D, Rauscher virus (RBL-5), and by dimethylbenzanthrene (EL. 4), and cells from mammary tumors (MM102), plasma-cell tumors (MPC-113), and fetal tissues. These results indicated that fetal antigens may be expressed in tumor cells, but they are different from tumor-specific antigens that are specific for a particular tumor or for tumors induced by a particular virus.

Animals↗

IL-4 regulation of perforin gene expression and BLT-esterase production in alpha CD3-induced activated killer cells.

This present study examines Il-4 regulation of perforin gene expression and cytolytic granule production in alpha CD3-induced activated killer cells CD3-AK. After stimulation of resting T cells with alpha CD3, proliferative response could be detected at 1 day after activation. The expression of perforin mRNA and production of cytolytic granules (using BLT-E as indicator) was detected on days 2-4, and this time course correlated with the generation of lytic CD3-AK cells. These findings indicate that killer cells generation is a late event during the course of alpha CD3 activation. Generation of CD3-AK cells is primarily PKC dependent and is blocked by the depletion or inhibition of PKC by PMA or SSP. These changes are accompanied by the suppression of perforin gene expression (mRNA) and BLT-E production. However, adding IL-4 into the cultures restored the perforin mRNA expression and BLT-E production, and also the cytolytic activity of the CD3-AK cells. Furthermore, for preactivated CD3-AK cells cultured in IL-2, SSP also suppressed the perforin mRNA and BLT-E with the concomitant reduction of cytolytic activity. Similar to the resting T cells, in the SSP-maintained preactivated CD3-AK cells, switching the cytokine from IL-2 to IL-4/IL-2 restored perforin mRNA expression and BLT-E production, with concomitant restoration of the cytolytic activity. In contrast, switching from IL-4/IL-2 gave the opposite effect. These results could be reproduced by using amiloride which also inhibited PKC activity but did not affect the growth of preactivated CD3-AK cells. These findings indicate that IL-4 may play a role in the late stage of alpha CD3 activation to regulate the expression of perforin gene and probably the translation process during the generation of activated killer cells.

Alkaloids↗