For the last 24 years, the Chern family has made a remarkable commitment to the postdoctoral fellows of The Wistar Institute. The Ching Jer Chern Memorial Award is given annually to the postdoctoral fellow who has written the most outstanding scientific paper in the previous year. The award was established in 1989 by June Chern in memory of her husband, Ching Jer Chern, who was a member of the scientific staff from 1974 until his death from cancer in 1987.
Each year, the recipient of the award conducts the Chern Memorial Lecture, an event attended by faculty, staff, and members of the Chern family. In what has become something of a family tradition, Mrs. Chern and her family take the opportunity to again donate to The Wistar Institute. This year, the Chern family generously supported the endowment with gifts of over $17,000 to Wistar.
“Postdoctoral fellows are the lifeblood of The Wistar Institute, and take a central role in directing research programs in each of our laboratories,” said Harold Riethman, Ph.D., a Wistar associate professor and associate director of training at the Institute. “The Chern Memorial Award has become a great honor for our fellows and it is a testament to the legacy of Ching Jer Chern and his family.”
This year’s winners, Haikun Wang, Ph.D., and Xiaoming Feng, Ph.D., (both of the laboratory of Wistar Assistant Professor Hui Hu, Ph.D.) were co-authors on the chosen paper, entitled “Transcription factor Foxp1 exerts essential cell-intrinsic regulation of the quiescence of naïve T cells,” which was published last spring in Nature Immunology. On June 22, Wang gave the annual Chern Memorial Lecture. Feng, who has gone on to establish his own research laboratory in China, was not on hand for the lecture.
The honored paper describes, for the first time, an amazing facet of the immune system, one that might be exploited to fight cancer and other diseases. For much of the time, our T cells—the white blood cells that act as the police of the immune system—are in a sort of “standby mode,” what immunologists call a "quiescent state." For years, scientists have wondered if quiescence occurred by default or whether T cells need to work at remaining silent.
Now, thanks to Hu and his team, there is direct proof that a protein, called Foxp1, actively maintains this standby mode in T cells until the cells are called upon by other parts of the immune system. "T cell quiescence has been a big mystery in immunology with some obvious and profound implications for treating illness by manipulating the immune system," said Hu.
Their findings could one day enable researchers to activate T cells to fight diseases such as cancer, which can go undetected or unrecognized by the immune system. In fact, the researchers report that knocking out the Foxp1 protein in mice activates T cells, allowing the cells to work in their policing function.