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Lupus Blog & Current Events

Interview with Dr. Ramirez-Ortiz

Friday, December 13, 2019
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I had the pleasure of interviewing our newest lupus faculty member, Dr. Zaida Ramirez-Ortiz. Zaida and I first met while we were postdoctoral research fellows at Mass General Hospital, and we've been friends ever since. In addition to being a scientific researcher, Zaida is an accomplished marathon runner and has competed in elite women's races all over the US.

1. Tell me a little about your career. I have a BS in General Biology with a minor in Microbiology from the University of Puerto Rico. I obtained my PhD from UMass Chan Medical School under the guidance of Dr. Stuart Levitz. The focus of my thesis dissertation was on immunity to fungal infections. Specifically, I studied the response of plasmacytoid dendritic cells (pDCs) activation mediated by Toll-like receptor (TLR) 9 to DNA from Aspergillus fumigatus. We were the first group to demonstrate the activation of pDCs and TLR9 by fungal pathogens. These molecules and cells also happen to be important for the inflammation that occurs in lupus.

After graduating from UMass, I transitioned to Massachusetts General Hospital for my postdoctoral training under the advice of Dr. Terry Means, where I worked on lupus models. My main project was to investigate the role of the scavenger receptor SCARF1 during inflammation. We demonstrated that SCARF1 is a novel apoptotic cell receptor that interacts with the complement receptor C1q bound to cellular debris. Furthermore, SCARF1-deficient mice develop lupus-like autoimmunity with symptoms similar to human disease such as the development of antinuclear antibodies, skin inflammation and nephritis. Currently, we are investigating whether SCARF1 on human cells plays a similar role as what we observed in our mouse system.

The second project I worked on during my postdoctoral fellowship was looking at the fine-tuning of the inflammatory response mediated by TLR7. We discovered the receptor TREMl4 as an essential positive regulator of TLR7. In the absence of TREMl4 we observed a reduction of the production of proinflammatory cytokines and autoantibodies in a lupus-prone mouse model. In addition, I have collaborated with a range of other labs resulting in multiple publications on these molecules in lupus.

2. What first got you interested in studying lupus? It wasn’t until I started to work on my postdoc project that I became fully interested in lupus. The two projects I worked on provided me with different views of the disease, such as the development of the disease and the molecular pathways that can potentially lead to treatment. I am particularly fascinated by the heterogeneity of lupus: no two patients look the same or have the same symptoms. 

3. What is your current research focus? Recently, I started my own laboratory at UMass Chan Medical School. The focus of my lab is the role of scavenger receptors during the inflammatory response in lupus. I plan to continue my work on SCARF1 and TREMl4 in addition to studying the role of TLR7 and TLR9 signaling and autoimmunity.

4. What do you think is the future of lupus? While there is no cure for lupus, we are currently working on developing new biomarkers for earlier diagnosis and new therapies. I believe that treatments for lupus need to be based on personalized medicine due to how heterogeneous the disease is.

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