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Estrogen-dependent switch tempers killing activity of immune cells
Date:8/10/2009

stored in granules (secretory lysosomes) in the cytotoxic T cells. They have greater quantities of these granules at their disposal once the blockage of the immune cells through EBAG9 is lifted.

These findings of the researchers in Berlin may also explain why drugs like tamoxifen act on tumor cell growth. One argument is that once the estrogen receptors of the tumor cells are inhibited by the drug, the sex hormone can no longer promote tumor growth. At the same time EBAG9 can no longer inhibit the cytotoxic T cells. The immune cells are ready to attack and destroy the tumor cells.

"In this way, tamoxifen not only inhibits tumor growth but may also be able to enhance the effect of the immune system," Dr. Rehm said. His working hypothesis is that EBAG9 acts as a molecular switch which regulates the immune cells.

As a next step, he and his colleagues plan to study cytotoxic T cells from patients with estrogen-dependent tumors to see if EBAG9 levels are increased.


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Contact: Barbara Bachtler
bachtler@mdc-berlin.de
49-309-406-3896
Helmholtz Association of German Research Centres
Source:Eurekalert

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