Meet the Researcher Monday: featuring Matthew Bettini, PhD.

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Dr. Matthew Bettini received his bachelor’s degree in Biology from Furman University in Greenville S.C. and then went on to earn his Master’s Degree in Biology at Georgia State University in Atlanta Georgia. After obtaining his Ph.D. from the Immunology and Molecular Pathogenesis program at Emory University in Atlanta GA, Dr. Bettini performed his postdoctoral training in the laboratory of Dr. Dario Vignali at St. Jude Children’s Hospital in Memphis TN.

In 2013, Dr. Bettini was recruited to Baylor College of Medicine/Texas Children’s Hospital in Houston TX, as an Assistant Professor within the Diabetes and Endocrinology section of the Pediatrics Department. At Baylor College of Medicine/Texas Children’s Hospital he was named a McNair Medical Institute Scholar in Type 1 Diabetes by the Robert and Janice McNair Foundation.

In 2019, Dr. Bettini was recruited to the University of Utah as an Associate Professor within the Microbiology and Immunology Section of the Pathology Department. The focus of Dr. Bettini’s research program is understanding central tolerance mechanisms and their dysregulation in autoimmunity. Currently funded projects are aimed at elucidating parameters of beta cell antigen specific T cell development, mechanisms important for tolerance induction to intestinal microbes, and cross talk between the gut and thymus in adults and neonates.

Why did you decide to become involved in type 1 diabetes research?
Believe it or not, T1D kind of picked me to be involved! In my early training at St. Jude Children’s Research Hospital, I came across a very unexpected result while studying the development of a type of immune cell, called a Regulatory T Cell. The main function of the Regulatory T cell is to suppress or regulate inflammation. It turned out that the protein necessary for the development of these cells wasn’t expressed very well in the mice I was studying and this led to a very rapid loss of their insulin producing beta cells and rapid autoimmune diabetes. I thought to myself, if these cells have that kind of power and control, I need to figure out how to make them better and stop autoimmunity from even starting. That idea launched my research program in T1D.

As a researcher, what are you most proud of?
This is a difficult question to answer. As a researcher in a University setting, my laboratory almost entirely consists of Ph.D. students. They drive the projects.  So, seeing my first graduate student earn his Ph.D. on the subject of Regulatory T cell development in Autoimmune Diabetes is still one of the top proud moments. I’d say a close second is being awarded funding by JDRF for pre-clinical tolerance studies to stop the initiation of T1D. This concept of stopping the initiation of T1D in susceptible individuals is my ultimate goal and being recognized by JDRF as a researcher worth funding is very humbling.

What is the greatest challenge you face in your research?
Honestly, being a successful small business owner (Consistent Funding). This is not unique to me. All University research programs are almost entirely funded by grants and grants can last anywhere from 1-5 years. From year to year, there can be dramatic swings in funding and a laboratory budget depending when a grant ends or starts. If a grant is not renewed or picked up, that means I may no longer have the funding to pay for all of my employee’s salaries or continue ongoing projects. This keeps me up at night.

What do you appreciate most about working with JDRF?
I was very fortunate to attend previous JDRF galas while working in Houston TX at Baylor College of Medicine and Texas Children’s Hospital.  What struck me about those events and the many others sponsored by JDRF is the laser beam focus on the children and their families. As a researcher attending one of those events, I always get a renewed sense of purpose. It may sound weird, but as a scientist, I do not get to interreact with those impacted on a daily basis by T1D, as physicians do.  Although, day in and day out it’s my goal to discover a means to stop the initiation of T1D, I’m removed from the personal connection to the disease. Working with JDRF establishes that bridge, that connection and invigorates my drive.

As a close friend of our local JDRF chapter, what can we do to help you in your research?
I am very fortunate to have a 1-yr grant funded by JDRF and a NIH-grant both focused on T1D. In the years ahead, I will continue to apply for funding to further my work towards a cure. I wonder if it’s possible to establish a directory or list of ongoing research for the local JDRF chapter, in case there is a desire by a kind donor to contribute to research in the state of Utah?

What would additional funding mean for your research?
The pre-clinical studies I have started with the JDRF Immunotherapy Innovative Grant allows me to test certain conditions but in order make any adjustments, the work will need to be continued past 1-year. Each experiment takes approximately 6 months to determine whether a therapy is working or not working.  Some of these experiments can be overlapping, but with others (higher/lower dose) we will need to wait and see what the results are first. Additional funding will allow for more conditions to be tested down the road.

What does a world without type 1 diabetes mean to you?
To me it means, the research community has delivered on its promise.

What is your favorite 80s movie?
Wow, can there be just 1? Warning, I am a child of the 80’s so my picks are skewed towards 5-14 year olds.

How about Favorite movie by year!

1980-Superman II, wasn’t allowed to see Star Wars

1981-Raiders of the Lost Ark

1982-E.T.

1983-Return of the Jedi

1984-Karate Kid (alternates: The Neverending Story and Ghostbusters)

1985-Back to the Future (alternate: Goonies)

1986-Ferris Bueller’s Day Off (Alternate: Stand By Me)

1987-RoboCop

1988-Die Hard (alternate: Blood Sport)

1989-Indiana Jones and the Last Crusade (alternate: Glory, Pet Sematary, Dead Poets Society)

Read Dr. Bettini’s publications:

Loss of Epigenetic Modification Driven by the Foxp3 Transcription Factor Leads to Regulatory T Cell Insufficiency

Ectopic Expression of Self-Antigen Drives Regulatory T Cell Development and Not Deletion of Autoimmune T Cells

A Critical Insulin TCR Contact Residue Selects High-Affinity and Pathogenic Insulin-Specific T Cells

Join us now to support the talented researchers at the University of Utah and drive the global scientific movement toward cures!