Researcher of the Month: Dr. Emily Wendt
3 questions to our scientist:
This month- Dr. Emily Wendt
Q: How did you get interested in your scientific work?
Born and raised in San Francisco, I studied Molecular and Cellular Biology at the University of California, Davis. A wonderful aspect of the Bay Area is the abundance of excellent research groups; during summer breaks I worked on research projects at UC Davis, UCSF, AstraZeneca and MedImmune. After my undergraduate studies, I joined ChemoCentryx, a start-up Biotech Company in Silicon Valley. At ChemoCentryx I used a variety of experimental techniques to evaluate the potency and specificity of chemokine receptor antagonists, with the objective of identifying novel therapeutics for the treatment of autoimmune and inflammatory diseases. Chemokines mediate immune cell migration and during inflammatory and autoimmune diseases there is exacerbated production of particular chemokines, causing immune cell infiltration and in the long-term, tissue damage. By blocking specific chemokine receptors, you can reduce the accumulation of immune cells in particular tissues without causing systemic immune suppression.
I quickly became interested in how these targets might advance patient treatment in the future. I decided that I wanted to follow the progression of medical research from drug discovery, through clinical trials and the evaluation of clinical results at a molecular and cellular level. I chose to pursue a DPhil at the University of Oxford to give me the experience of living abroad, and to participate in the translational research that is now the hallmark of the Translational Gastroenterology Unit (TGU).
Q: What are you working on now?
Last summer I completed my DPhil in Clinical Medicine, under the supervision of Dr Keshav, studying the role of chemokine receptor 9 (CCR9) in intestinal inflammation. I am currently completing a postdoctoral project in Dr Keshav’s lab, characterizing leukocyte populations that express CCR9 and other ‘gut homing’ molecules, including β7 and α4β7 to identify differences in Ulcerative Colitis (UC) and Crohn’s disease (CD) – the two diseases that comprise Inflammatory Bowel Disease (IBD). There is huge excitement in IBD research about new therapies that target these gut specific molecules, as they may allow more targeted treatment with fewer side effects. An extremely interesting observation is that these and other commonly used treatments have been successful in either UC or CD, but rarely both. Although there have been important advances in our understanding of IBD, the pathogenic cell population(s) remain unknown, and it is likely that difference between UC and CD exist. I hope that by examining IBD in reverse, studying the effects of successful therapeutic interventions and asking what has changed in the cell populations present in the gut, I might help advance our understanding of a complex and challenging disease.
Q: What do you enjoy most about working in science?
I have really enjoyed the process of identifying an unexplained problem, formulating a hypothesis, and then designing novel approaches or techniques to tackle the question. For example, during my DPhil I designed a technique for measuring intracellular calcium flux in minority cell populations. Using this technique I was able to confidently measure the effects of drug treatment on a small population of primary derived cells. I have also enjoyed being a part of the diverse and wonderful community of scientists I have met at Oxford and the TGU in particular. Working with a group of exceptional scientists and clinicians from a variety of backgrounds has been an invaluable source of inspiration and learning.