Influenza viruses infect the cells lining surfaces of the respiratory tract. Once they have entered these cells, the viruses highjack the genetic machinery to produce more copies of their own RNA and generate more viruses.
A research team headed Dr. Xiaoping Liu at the University of Maryland, along with scientists at Synbiotics in College Park, Md., China Agricultural University in Beijing, California Institute of Technology in Pasadena, and The Jackson Laboratory, now show that by pairing with a special receptor, known as FcRn, antibodies can enter cells that have been invaded by influenza virus and shut down their replication machinery. The research results were published in the Proceedings of the National Academies of Science.
The researchers, including Jackson Professor Derry Roopenian, showed that mice lacking FcRn were not able to fend off influenza infection even when given influenza-specific IgG antibodies before infection, whereas normal mice were. If all the infection-fighting occurred outside the cells, FcRn would not have been necessary for a successful immune response.
A better understanding of how—and where—the antibodies fight viruses is important for designing new and more effective vaccines and antibody-based therapies.
The Jackson Laboratory, founded as a cancer research center in 1929, is a nonprofit biomedical research institution and National Cancer Institute-designated Cancer Center based in Bar Harbor, Maine. Its mission is to discover the genetic basis for preventing, treating and curing human diseases, and to enable research and education for the global biomedical community.
Bai et al.: Intracellular neutralization of viral infection in polarized epithelial cells by neonatal Fc receptor (FcRn)-mediated IgG transport. PNAS early edition, Oct. 31-Nov.4, 2011.
Joyce Peterson, 207-288-6058, The Jackson Laboratory
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