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Penn researchers describe key molecule that keeps immune cell development on track
Date:8/8/2011

hey will express TCF-1 and take on other features of T cells," says Chi.

However, when they forced expression of TCF-1 in cells using retroviruses, Weber noticed expression of T-cell proteins on the surface of cells -- even when Notch signals were absent. The team further characterized these new T-lineage cells by looking at gene expression on microarrays and found they expressed many T-cell specific genes. They concluded that Notch normally turns on TCF-1 early in development, and that TCF-1 then does the job of turning on T-cell genes and keeps T-cell maturation on the right track.

"The data are telling us that Notch delegates much of its work during T-cell development to TCF-1," says Bhandoola, "But we now have many questions about what comes next."

Adds Weber, "Some of the new questions are: How is TCF-1 regulated after Notch steps off stage? What keeps it on? What is TCF-1 doing? And how is it doing it?"

In many clinical settings, early T-cell progenitors are likely to be deficient, especially in patients undergoing bone marrow or blood-cell-producing stem cell transplantation situations in which new T cells fail to be produced for long periods of time. In some patients, especially elderly ones, there is never true recovery of T cells, and this non-recovery can be associated with infection.

"To improve the outcome of transplant patients, the process of T-cell development needs to be better understood," says Chi. This may also be important in cancer patients who get profound immunosuppression from treatments and in AIDS patients when T cells are not made at a rate sufficient to replenish the T-cell pool.

"It's possible that one day we will use molecules like TCF-1 to improve T-cell development for people," says Weber.


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Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
Source:Eurekalert

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