The immune system declines with age, its army of cells capable of meeting new threats diminishing in number and capacity. One possible form of palliative therapy for immune system aging, intended to produce benefits to the condition of the patient without addressing the underlying causes of this degeneration, is to create large numbers of new immune cells and infuse them into the patient. It is well within the present capabilities of the stem cell research community to grow new immune cells from a patient's stem cells - and indeed this has been accomplished for some years in various forms of clinical trial.
Here is a study that tries this sort of approach in mice, but with mixed results: no harm is done, and it looks like the therapy is having the intended effect under the hood, but equally the most obvious measure of whether it's doing any good in terms of boosted immune response isn't reliably improved either. More work is needed here:
Transfusion of autologous leukocytes after prolonged storage has been proposed as a means of rejuvenating the immune system of older individuals. The rationale for this approach is that age related immune decline is associated with a diminished pool of naïve T cells following atrophy of the thymus and reduction in thymic output. The presence of high levels of naïve T cells within the blood of young individuals could provide a boost to the immune system of an older "self" through a rejuvenation of the naïve T cell pool.
However what remains unresolved is whether the cells could be incorporated effectively into the T cell pool of the host and whether effectors could be generated. Using CD45 congenic mice in our experiments we show that the transfusion of young donor cells into older congenic host animals leads to their successful incorporation into the peripheral T cell pool. When the recipients were challenged with influenza virus, specific effector CD8 cells were generated which were of both host and donor origin.
This would suggest that the environment provided by the host is not lacking and that effectors could be generated in an immune response to antigenic challenge. However the functional response as judged by viral load would appear to be variable, muted in some animals and showing greater effectiveness in others. Our results reveal that although there was a five-fold difference between the lowest and the highest number of cells transferred, at the time of assay there was no major difference in the numbers of donor cells in the hosts when compared with the numbers injected. Our experiments would suggest that there appears to be no direct correlation between the number of cells injected and the number of cells present within the host at the time of assay, implying that cell dose was not a critical factor in incorporation into the peripheral T cell pool.