Many autoimmune immune diseases are caused by T cells, which normally fight threats such as viruses, bacteria, and even cancers. T cells develop in an organ called the thymus, where they learn to recognize threats.

LJI Professor Hilde Cheroutre, Ph.D., is studying this T cell education process. Her lab is interested in how autoreactive T cells learn to target “self.” These “educated” autoreactive T cells are actually helpful sometimes. They can even help the body by regulating immune responses to cancer cells or infected cells. But under the wrong circumstances, a naïve T cell may encounter a specific target (called a self-antigen) and spark an autoimmune response.

Dr. Cheroutre and her team are working with doctors at Rady Children’s Hospital-San Diego to better understand how this process goes wrong. The team hopes to be able to identify the signs that an infant might be susceptible to autoimmune diseases and perhaps even prevent autoimmunity altogether.

LJI scientists have also received significant support from the Global Autoimmune Institute (GAI) to investigate the beginnings of autoimmune disease processes. In 2024, GAI granted funding to LJI faculty member Sam Myers, Ph.D., who now serves as LJI’s Global Autoimmune Institute Assistant Professor.

Investigating important genes

LJI scientists are also using cutting-edge tools to understand links between our genes and autoimmune disease. In 2025, LJI Professor Anjana Rao, Ph.D., and her colleagues investigated how cell function is manipulated by small pieces of DNA called “transposable elements.” These pieces of the genome are normally silent in healthy cells, but under many pathological conditions they can “wake up” and occasionally even “jump” into our regular genetic code. Rao’s study showed how cells assemble a protein network to suppress transposable elements. These protein networks may help protect against harmful genetic rearrangements and prevent the development of autoimmune disease.

Meanwhile, LJI Professor, President & CEO Erica Ollmann Saphire, Ph.D., MBA, is zooming into HERVs, which are pieces of viral DNA that got trapped in the human genome long ago in our evolutionary past. These viral genes can “awaken” during autoimmune disease development and may contribute to immune cell dysfunction. Dr. Saphire’s lab is advancing research into HERVs through structural studies that reveal the 3D architecture of viral proteins. This work is an important step toward developing therapies that may counteract immune cell dysfunction.

LJI Associate Professor Sonia Sharma, Ph.D., is studying inflammatory and autoimmune diseases that affect the vascular endothelium, the cells lining the blood vessels. Her laboratory integrates cutting-edge genetics, biochemistry, cell biology, computational and translational approaches to define the key genetic mechanisms regulating cellular innate immunity—and determine how these factors can trigger autoimmune disease.

LJI Professor Michael Croft, Ph.D., studies molecules involved in causing atopic dermatitis, severe asthma and fibrotic diseases caused by chronic inflammation. He has partnered successfully with several companies and his work has led to clinical trials for asthma and atopic dermatitis. 

LJI Professor Mitchell Kronenberg, Ph.D., is investigating how surface molecules and intracellular signaling pathways regulate immune cells that reside in the intestine.  These immune cells have a unique challenge because they must co-exist with a highly diverse microbiome. He studies how these cells maintain this peaceful co-existence while responding to pathogens. The loss of tolerance of good bacteria is a key step involved in the pathogenesis of inflammatory bowel diseases (IBD), such as Crohn’s disease and ulcerative colitis.

LJI Professor Alessandro Sette, Dr.Biol.Sci., has also teamed up with LJI Professor Bjoern Peters, Ph.D., to build the Immune Epitope Database (IEDB), a publicly available online resource that includes data from researchers around the world. The IEDB is a valuable tool for studying the chemical aspects of what immune cells recognize when they make an immune response, including when they mistakenly target a person’s own organs in different autoimmune diseases.