Ramiah Jacks, Ph.D., a postdoctoral fellow in the lab of Carey Lumeng, M.D., Ph.D., was recently designated an NIH MOSAIC Scholar and had her work featured at the inaugural U-M Medical School Deans Lecture series. In this profile, we get to know more about her path to U-M and her research focus.
How did you develop your interest in biomedical research?
Ever since I was in high school, I knew I wanted to do research because I was so interested in understanding how our body works. I went to DePaul University in Chicago where I was able to do research as an undergraduate and that sparked the joy of discovery for me.
I decided to go to grad school at Loyola University in Chicago, where I did immunology research on the function of T cells and how certain cytokines can dictate T cell fate and function. I really loved the application of learning small bits of information and building a complete story of how we can add to our knowledge of how our immune system works and how our body works. I really wanted to continue doing research, but realized I also I loved teaching and mentoring, talking to students, encouraging them and helping to guide them to their next steps.
What brought you to U-M?
I found the NIH’s Institutional Research and Academic Career Development Awards (IRACDA) (K12) program, I applied at U-M because it’s a program designed to foster the growth of individuals who want to stay in academia, do research but also want to teach.
Under my advisor Carey Lumeng in the Department of Molecular & Integrative Physiology, I’m able to continue my research, but I also am learning a lot from the Center for Research on Learning & Teaching, specifically, best practices for teaching for equity and inclusion and also linked up with individuals aligned with ideologies about increasing diversity, equity and inclusion in the laboratory as well as the classroom.
You presented at the recent U-M Medical School Deans Lecture event, which focused on research about inflammation. What specifically are you studying?
One thing we know about obesity is there’s what’s called obesity associated inflammation within the adipose tissue, which is associated with insulin resistance and metabolic disorders in mouse models as well as humans. Dr. Lumeng’s lab is really trying to understand how inflammation within adipose tissue occurs. With my background in T cell research, I wondered what was going on with the T cells and took on that project.
In mice and humans with obesity, the T cells are exhausted, meaning they’ve been activated so long they can no longer function properly. My question is how do they get to that state? We know what happens at the end, so I wanted to know what happens at the beginning.
Within adipose tissue specifically, inflammation can have a negative connotation but that isn’t necessarily the case. There are immune cells required for homeostasis, especially in lean, healthy adipose tissue. The real question for our lab is why is there a switch from the good immune cells present in lean states to the more inflammatory, damaging immune cells in obese adipose tissue.
Tell us more about your experiment.
I’m using a short-term high fat diet model where mice are placed on a 60% high fat diet (HFD) for 1 or 2 weeks to observe what is happening with T cells. I noted proliferation of T cells in adipose tissue and when I dived further into what subtype of T cells are proliferating, I identified that it’s the memory T cells. Memory T cells are T cells that have be previously activated by an antigen and have developed a memory program so that they can more rapidly respond when they see that same antigen again compared to naïve T cells. Activation of these memory T cells in the presence of HFD could help orchestrate the adipose tissue inflammation we see with obesity.
The biggest gap in the field is determining what that antigen is. I’ve hypothesized there is an antigen and am trying to devise ways in which to assess what it is. These memory T cells are already present in adipose tissue even in lean mice that have never been on a high-fat diet so I’m asking how they got there and what are they reacting to. I propose that perhaps these T cells were formed via a self-antigen expressed in our body that has a structural similarity to an antigen that’s expressed or presented when you place mice on a high fat diet. And because of that cross reactivity, we get activation of a subset of memory T cells.
You were recently designated an NIH MOSAIC Scholar. Can you tell us more about that?
The MOSAIC (Maximizing Opportunities for Scientific and Academic Independent Careers) is a relatively recent award. The NIH K99/R00 award mechanism has been around for a while and supports researchers in the transition award from postdoc to your professorship/faculty position.
The MOSAIC award recognizes the fact that individuals who want to promote diversity and increase diversity in academia have what’s called a diversity tax. We’re doing more work outside of our research, but we’re also not getting recognition or rewarded for work that is extremely important. The MOSAIC award recognizes and encourages this effort. When I saw the award, I thought to myself this aligns perfectly with what I want to do. My advisor encouraged me to apply so I applied, and I got it and am really happy to have received it.
I know for myself that one of the reasons I stayed in science so long is because I had a village and community of mentors really guiding and encouraging me. I think that sense of belonging really is so important especially for individuals of minoritized backgrounds to continue to do the work to stay in this field.
I had a lot of friends with relatives or parents who were scientists and as a result, they knew exactly what to expect and could go to them for issues or to vent. I didn’t have those opportunities. I had my teachers, mentors and advisors that really encouraged and helped me, and I want to be a part of that village for the next student. I’m going to make a laboratory and classroom environment that is welcoming and encouraging for all students, including those who look like me because oftentimes, I didn’t feel like I belonged. I want to be a part of the solution.