Center for Human Cell Therapy Boston Awarded 5 year Production Assistance for Cellular Therapy (PACT) contract by the National Heart, Lung and Blood Institute to advance cell therapy research
Cristian Boboila and Tingting Zhang, two immunology graduate students in Fred Alt's laboratory have just published a complementary set of three papers that provide major new insights into mechanisms of antibody class switch recombination and DNA repair. Two of the studies, one led by Tingting Zhang and the other by Cristian Boboila, will appear back to back in an upcoming issue of PNAS.
By studying how inflammation and cytokines control stimulation of perforin gene activity in CD8 T cells, Matthew Pipkin in the Rao lab has shown in a recent Immunity paper that effector and memory CTL development are controlled by a complex interplay between inflammation and the cytokine Interleukin 2.
The primary mode of calcium entry in lymphocytes involves a “store-operated” calcium channel known as the CRAC channel, which consists of ORAI and is opened by the calcium sensor STIM. The Hogan lab used a clever strategy to show that a purified recombinant STIM fragment suffices to open ORAI channels expressed in yeast vesicles.
In people, mature B cells can last a lifetime, hanging around even when they are not actively producing antibodies for an ongoing immune response. This endurance of resting B cells is important for mounting a rapid response to new threats, and gives us the immunological memory that makes vaccines so effective.
Too much clotting can cause stroke or heart attack; too little can make a person bleed to death. The length of the blood clotting protein von Willebrand factor (VWF) sets the correct threshold. Using tiny laser "tweezers” to hold single molecules, researchers co-led by Timothy Springer, PhD, of PCMM/IDI showed that the A2 domain of VWF acts as a force sensor that unfolds in response to blood flow, and then is cleaved, enabling the correct balance to be struck between bleeding and clotting.
"We are delighted at this opportunity to join forces with such a high-caliber team of researchers who share our interest in finding answers to some of the most vexing diseases, from lupus to diabetes to various cancers," says James Mandell, M.D., Chief Executive Officer of Children's Hospital Boston.
Whether condoms or abstinence, most efforts to prevent sexually transmitted diseases have a common logic: keep the pathogen out of your body altogether. While this approach is certainly reasonable enough, it doesn’t help the countless people worldwide who, for a number of reasons, are not in a position to control their sexual circumstances.
Image courtesy of Cell Host & Microbe, Judy Lieberman, January 22, 2009
Pictured: Cholera toxin (red) internalization in several mammalian epithelial cell lines proceeds via vesicles and tubules from the plasma membrane towards the perinuclear endosomal/Golgi area. Representative confocal images from middle sections of cells are shown.
Denisa Wagner, Ph.D., and colleagues have shed light on the regulatory powers of a molecule called CalDAG-GEFI. Pictured: A micrograph of a small, injured blood vessel shows fibrin deposition (dark areas) that prevents leakage of blood into surrounding tissue.
Researchers at the Program in Cellular and Molecular Medicine and the Immune Disease Institute at Children's Hospital Boston (PCMM/IDI) have found a link between a common mutation that can lead to cancer and a distant gene regulator that enhances its activity. Discovery of this relationship could lead to drugs targeting B-cell lymphomas, including Burkitt's lymphoma, an aggressive cancer in children, as well as multiple myelomas and other blood-related cancers.
Lymphomas often originate in B cells, the same cells that produce antibodies to help fight infections. A B cell can become cancerous if a gene known as c-myc leaps to another section of DNA (the IgH region, responsible for building antibodies), fuses with it, and somehow becomes over-activated. Scientists have wondered for years how this oncogenic activation occurs, in particular what component in the IgH region activates c-myc. The new study, published in the Dec. 10 issue of Nature, identifies this regulatory… Read More »
On January 15th 2010, Dr. Leslie E. Silberstein of the Center for Human Cell Therapy Boston (CHCT) at the Immune Disease Institute was awarded a Production Assistance for Cellular Therapies contract… Read More »
Press Release - Max Delbrück Center for Molecular Medicine
The German immunologist Professor Klaus Rajewsky from Harvard Medical School in Boston, USA, has received the… Read More »