Julia Hurwitz Lab

When you vaccinate someone, how does the immune response work? When someone is challenged by a viral or bacterial infection, what occurs in the immune system? How are B cells triggered to make antibodies and how are T cells triggered to kill infected cells? These questions drive our study of the body’s immune response.

Most recently, our work examines nuclear receptor ligands, which include vitamins A and D, sex hormones (estrogen and testosterone), thyroid hormones, and prednisone. Since these ligands influence B and T cell responses to viruses, bacteria, and vaccines, we ask how they regulate pertinent genes including immunoglobulin and T cell receptor genes. We use chromatin immunoprecipitation (ChIP) and single-cell studies to learn how nuclear receptor ligands and their corresponding nuclear receptors bind DNA and thereby influence the immune response.

The major focus of our laboratory is vaccine development. We direct our vaccine development efforts toward viruses such as parvovirus—the cause of aplastic crisis in children with sickle cell disease—and HIV. Some of our most exciting, recent work pertains to the development of a Sendai virus vector that serves as a two-for-one vaccine. The vaccine targets parainfluenza virus type 1 (PIV1)—the cause of croup in babies—and respiratory syncytial virus (RSV). The National Institutes of Health (NIH) is currently testing this vaccine in humans.

We also conduct research in an exciting, and highly publicized, arena of vaccine development that focuses on mRNA technology. We currently work to apply the mRNA platform to combat a number of different pathogens.

By combining our B cell and T cell research, our study of environmental factors that impact the immune response, and our comprehensive vaccine development effort, we are able to advance prophylactic approaches to manage infectious diseases in children.