Emily Moser, PhD

Influenza A virus is a serious global health threat, causing approximately 36,000 deaths per year in the United States alone. The primary intervention against influenza infection is vaccination to induce protective antibodies. Programming of the antibody response occurs in specialized niches in lymphoid tissue called germinal centers. Vaccines are less effective in certain groups with weakened germinal center responses, such as elderly and immunocompromised individuals. We have discovered that the enzyme Cul4b is essential for germinal center expansion and formation of protective antibody responses. Our research will define the role of Cul4b in germinal center and antibody responses after influenza vaccination. Results from these studies will aid in the design of new vaccines that enhance the Cul4b pathway, unleashing robust antibody responses in populations with weakened immune systems.

Update:
We have discovered a novel pathway in immune cells called B cells that promote protective immunity against influenza A virus. The enzyme Cul4b promotes antibody formation after both infection and vaccination with influenza virus. Our latest results show that B cell Cul4b promotes proliferation and survival after DNA damage associated with somatic hypermutation, a process that allows B cells to mutate the genes that they use to produce antibodies. In this way, Cul4b facilitates strong-bonding antibody formation, rapid virus clearance, and long-term protection.