Ronald B. Corley, PhD
Professor and Chairman of Microbiology, Associate Director of NEIDL Institute
BS, Duke University
PhD, Duke University
Our laboratory is interested in the relationship between innate and adaptive immunity, and how components of the two discrete systems interact to generate long-lasting protective immune responses. One area of focus has been on the role of IgM antibodies as efficient bridges of innate and adaptive immunity. Mice that are deficient in secreted IgM have a number of immune defects characterized by their inability to respond to low concentrations of protein antigens, delayed production of protective antibody responses to pathogens, and delayed germinal center formation. In the absence of secreted IgM, pathogens also fail to concentrate into secondary lymphoid organs and instead disseminate into vital organs. We have demonstrated an “adjuvant” role for IgM, and the function of IgM can be attributed, at least in part, to its ability to concentrate immune complexes in the foci of the spleen, where innate B cells in the marginal zones traffic the complexes to follicular dendritic cells, stromal elements that promote efficient germinal center formation. These functions require native organization around the marginal sinuses for efficient adjuvant effects of IgM.
The laboratory also focuses on the immune consequences of infection with highly pathogenic hemorrhagic fever viruses, including filoviruses. Patients infected with these viruses often fail to make adaptive immune responses and succumb to infection. While this is often attributed to dysfunctional innate immune responses, the nature of the defects in immune responses to these viruses is poorly understood. We have initiated studies to dissect the early immune responses to these viruses, understand how they affect the ability of infected animals to initiate adaptive immune responses, and identify the components of infection that lead to the cytokine storms that characterize infection with these viruses.