Innate Cells Shown To Form Immunological ‘Memory’ And Protect Against Viral Infection
Innate memory provides protection against vaccinia
Researchers have demonstrated that cells of the innate immune system are capable of “memory”, and of mounting rapid protection to an otherwise lethal dose of live vaccinia virus. The study, published in the Open Access journal PLoS Pathogens on August 4th, challenges previous thought that only B cells and T cells can store memory to ward off future infection. The finding, by researchers from Beth Israel Deaconess Medical Center, Harvard Medical School, and Hebrew University and Duke University, has potentially significant consequences for the design of future vaccines, particularly for HIV.
Immunological “memory” is what the immune system builds to respond more effectively to pathogens (such as bacteria and viruses) that the host organism has encountered previously. Traditionally, immunological “memory” has been thought to reside within the cells of the adaptive arm of the immune system (B cells and T cells) that recognize highly specific portions of pathogens through unique receptors.
This study, lead by Dr. Geoffrey Gillard, shows that an innate population of cells, called natural killer (NK) cells form “memory” to vaccinia virus infection despite the fact that they lack the receptors of traditional “memory” cells. Transfer of “memory” NK cells into immunodeficient mice was enough to protect these mice against a normally lethal exposure to vaccinia virus. Because the NK cell population lacks the receptors that allow B and T cells to develop highly specific “memory” responses to pathogens, the study raises important questions to the manner in which “memory” NK cells are capable of recognizing virus upon a second exposure.
Understanding how innate “memory” functions will be critical for incorporating this property into more effective vaccines, particularly as part of a vaccine against HIV. The properties of NK memory, most notably the ability to respond very rapidly, may be helpful in exerting early control of HIV infection by limiting the ability of the virus to overwhelm the host immune system in the early stages of infection.
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