A recent research from the Trudeau Institute, Saranac Lake, New York, shows that the immune system cells that are essential both for vaccine efficacy and pathogen resistance to live more in older animals but due to this longevity acquire functional shortcomings. The study may offer fresh targets to boost the immune system function in elderly people.
The immune system function is a well-documented one. It accompanies the aging process and leaves older people more vulnerable to various infectious agents compared to younger individuals. As a result, several vaccines that are currently in use are not quite as efficient in protecting elderly people. For instance, the Journal of the American Medical Association research discovered that in people above seventy years old, the influenza vaccination provided a protection of only 23 percent and decreased reactions have also been witnessed for tetanus and hepatitis vaccinations.
Susan Swain, a Trudeau Institute Investigator along with her colleagues have in previous work shown that a particular kind of immune cells, known as CD4 T cells, which are vital for vaccine response, tend to become less effective as one ages. Vigorous CD4 activity is essential for the production of antibodies in response to vaccination or infection. (The immune system comprises of a number of varied kind of cells including B cells that produce several classes of T cells and antibodies. CD4 T cells are a kind of helper cell that triggers the production of B cell and various other components of immunity.) Particularly, “naive” CD4 T cells, those which have not come into contact with or have become expert in responding to a specific pathogen, are required to make sure that there is protection against novel pathogens in addition to robust responses to vaccination.
In a recent study, which was published in October in the Proceedings of the National Academy of Science, Susan Swain demonstrated that naive CD4 T cells of older mice lived more than the matching cells obtained from young mice when it was transferred into normal intact hosts. This result makes it easier to explain the way older animals sustain populations of circulating CD4 T cells, although generation of novel cells in the thymus declines radically with age. Susan Swain and her team have demonstrated that cells that are older were comparatively resistant to cues that initiate a process called apoptosis (from Greek “falling leaves), a kind of coordinated cell death, and that these cells have lesser levels of a molecule that supports apoptosis.
However, although older CD4 T cells benefit from a longer lifespan, their function deteriorates. The study that Swain and her team conducted illustrates that this degeneration of their function and the longevity seem to be connected, with the start of longer life-span preceding the functional defects. Since age puts the cells in exposure to rising levels of stressors like oxidative damage (aka “free radicals”), which encourage alterations linked with cancer, the authors hypothesize that the strategy of sustaining CD4 cells numbers by increasing the lifetime of individual cells rather than be encouraging the propagation of new cells may be a defence of sorts against the development of tumour.
This speculation remains yet to be examined furthermore, but, through future study that will also be directed towards unveiling the linkage between the lifespan of cells and the degeneration of their function in an effort to develop ways of enhancing CD4 activity, and hence vaccine efficacy and pathogen resistance in elderly people.
Source: eurekalert
Anti Aging, Bioscience, Gerontology, Health And Aging, Longevity
Sat, Jun 5, 2010
Anti Aging, Bioscience, Gerontology, Health And Aging, Longevity