In a report published in the 4th August issue of the Open-Access journal PloS Pathogens, researchers showed that cells in the innate immune system store “memory” that enables them to elicit a rapid protective immune response to a dose of live vaccinia virus, which is otherwise considered lethal. The study attempts to challenge a former belief that only B and T cells are capable of storing memory to combat future infections.
This novel discovery that will have a potentially critical effect on the design and development of future vaccines, HIV in particular, was made by researchers from Beth Israel Deaconess Medical Center, Harvard Medical School, Hebrew University and Duke University.
When a host organism encounters pathogens, such as bacteria and viruses, the Immune system builds an Immunological “memory” with the intention of combating the same pathogen more powerfully during a second encounter. Traditionally, only B cells and T cells (cells of the adaptive arm of the immune system) were believed to have Immunological “memory.” These cells act by exposing highly specific pathogen fragments through unique receptors.
Despite lacking traditional “memory” cell receptors, natural killer (NK) cells (an innate population of cells) are capable of storing “memory” for vaccinia virus infections, said study lead Dr. Geoffrey Gillard. Immunodeficient mice were protected against an otherwise lethal dose of vaccinia virus due to the transfer of “memory” NK cells.
Unlike B and T cells, the NK cell population has no such cells that can develop highly specific “memory” responses to pathogens; hence, the study pinpoints a very essential question regarding how “memory” NK cells identify viruses upon a second encounter.
Harnessing this property to create more effective vaccines, specifically for HIV, will necessitate an in-depth understanding of the working and functionality of innate “memory.” This remarkable property of the “memory” NK cells that allows for a rapid and efficient response could be exploited to control early stage HIV infection by limiting the virus’s ability to overthrow the host immune system.