Scientists from the Department of Medicine have recently published major advances in our understanding of a number of important diseases including inflammatory bowel disorder, rheumatoid arthritis, malaria, recurrent respiratory and virus infections. READ MORE
Scientists discover genetic disease which causes recurrent respiratory infections
Discovery could lead to new treatments for this genetic disorder
Cambridge scientists have discovered a rare genetic disease which causes severe respiratory infections and lung damage. Because the scientists also identified how the genetic mutation affects the immune system, they are hopeful that new drugs currently undergoing clinical trials to treat leukaemia might also be effective at helping individuals with this debilitating disease.
For the study, led by the University of Cambridge in collaboration with the Babraham Institute and the MRC Laboratory for Molecular Biology. The researchers, who were primarily funded by the Wellcome Trust, MRC and the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre, found that the mutation increases activity of an enzyme called Phosphoinositide 3-Kinase δ (PI3Kδ). The enzyme is present in the immune cells, where it regulates their function. However, constantly activated PI3Kδ impairs work of these immune cells, preventing them from efficiently responding to infection and providing long-lasting protection. As a result, patients with this mutation have severe and recurrent infections. The paper was published in Science by joint senior authors Sergey Nejentsev and Alison Condliffe from the Department of Medicine.
Researchers discover that the cells play a major role in inflammation which underlies Crohn’s disease in small intestine.
Crohn’s disease, the inflammatory bowel disorder, can originate from specialised intestinal cell type called Paneth cells. Timon Adolph, Arthur Kaser and their co-authors propose that small intestinal Crohn’s disease might be a specific disorder of this cell type, providing a possible new target for treatments. The study was published today in the journal Nature and was featured on Cambridge University Research News.
“If we are able to break down Crohn’s disease into subsets by understanding the underlying mechanisms, which we have done here, we hope to develop much more targeted, effective treatments. “
Researchers have identified a gene that seems to control the pathways that drive the development of Crohn’s disease and rheumatoid arthritis. The work was recently published in the Journal Cell.
The international team, led by Ken Smith at the Cambridge Institute for Medical Research at the University of Cambridge, looked at existing data from genome-wide association studies in Crohn’s disease to focus on prognosis rather than diagnosis. They identified a variant in the FOXO3A gene that is associated with the outcome of Crohn’s disease but not associated with its diagnosis.
Researchers have identified a crucial interaction between cells of the immune system after acute myocardial ischemia and this work identifies new therapeutic targets for acute myocardial infarction. The findings were recently published in Nature Medicine by senior author Ziad Mallat and his team and international collaborators.
Human Cytomegalovirus the silent killer?
Researchers have discovered a new target that may allow us to target and eliminate cells that are latently infected with a virus. Many of us are infected with human cytomegalovirus that we’ll never clear. While we’re healthy, it’s nothing to worry about, but when our immune system is suppressed it could kill us.
Researchers have started to identify major changes in these latently infected cells, and think these are targetable with novel drugs and immunotherapies.v“One change is in a transporter protein normally used by the cell to pump out things it needs to get rid of,” he added. “If you put the chemotherapy drug vincristine on a healthy cell, the cell will pump it out and survive. John Sinclair from the Dept of Medicine with Paul Lehner at the Cambridge Institute for Medical Research we found that, during latent infection, this transporter protein is less effective, making the cell more prone to killing by vincristine.” Their results were published in Science.