Could aging partially be due to an acquired autoimmune disease

For my Ph.D. work I wrote a paper about how part of the aging process may be due to a type of acquired autoimmune disease. The paper suggests that over time the immune system must continually interact with stem cells that have acquired mutations and have become cancerous. Even normal people without cancer develop many cancerous cells throughout their lifetime. These "normal" people just don't notice this because their immune system is able to take care of the problem early enough. If the immune system must continually fight these aberrant stem cells over a long period of time, then I hypothesize that the immune system may fail to distinguish between healthy stem cells needed for repair and cancerous stem cells. In my paper, I outline several experiments which could be performed to test this hypothesis. I also provide some useful information about aging in general.

Here's a link to the paper: http://www.scribd.com/doc/33702865/Role-of-Immune-Recognition-of-Stem-Cells-in-the-Aging-Process
Here's the first paragraph from the paper:
Stem cells are among the many different types of cells in the body which can become cancerous through processes of mutation, chromosomal instability, and changes in gene regulation. One of the requirements that must be met in order for a cell to become cancerous is that it must be able to overcome the Hayflick limit presented by the end replication problem of eukaryotic cells. In order to overcome this limit, a cell must either express telomerase or develop an ALT (alternative lengthening of telomeres) mechanism. Since stem cells naturally produce the enzyme telomerase, they already meet one of the requirements for becoming cancerous and are just a few mutations away from becoming malignant. Over the course of a lifetime, the immune system of an individual may have suppressed such rogue stem cells many times. If the immune system incorrectly associates normal proliferating stem cells with these cancerous stem cells, the ability of the organism to repair itself will degrade which may eventually lead to death. With this research, we aim to test the unconventional hypothesis that the aging process may be a type of acquired autoimmunity against stem cells.


I also describe an additional experiment to test this hypothesis which involves measuring the wound healing rates of mice with and without immune systems in old age. Theoretically, if the immune system does pose a problem to stem cells in old age, then the mice lacking an immune system should heal faster when injected with stem cells than normal mice when injected with stem cells.

Here's a link to the paper: http://www.scribd.com/doc/33703156/Wound-Recovery-With-Hematopoietic-Stem-Cells-in-SCID-and-WT-Mice-at-Different-Ages
Here's the first paragraph from the paper:
If the immune system fails to distinguish between cancer stem cells and healthy stem
cells in old age, then mice with severe combined immune deficiency (SCID) would be
expected to recover from a wound healed by young hematopoietic stem cells more quickly
than wild type (wt) mice treated with the same stem cells. The general experimental setup
will involve wounding mice of two different age groups, and determining if there is a difference
in wound healing rates among scid, wt, stem cell treated, and non-stem cell treated mice.
The rate of wound healing will serve as an approximate quantitative measure of the aging
process, which results in a decreasing ability to repair damage over time. The observation
that the stem cell treated scid old mice do not heal significantly faster than stem cell treated
wt old mice would suggest that the proposed hypothesis is incorrect. In other words, this
observation would suggest that the immune system does not inhibit the healing process and
is not failing to distinguish between cancer stem cells and healthy stem cells in old age.