There is considerable support for destroying and recreating immune cell populations to deal with autoimmune diseases and some aging effects. For example, for B cells:<p>----<p>1) Reversing B cell aging<p><a href="http://www.impactaging.com/papers/v3/n4/full/100313.html" rel="nofollow">http://www.impactaging.com/papers/v3/n4/full/100313.html</a><p>2) Long-lived autoreactive plasma cells drive persistent autoimmune inflammation.<p><a href="http://dx.doi.org/10.1038/nrrheum.2011.1" rel="nofollow">http://dx.doi.org/10.1038/nrrheum.2011.1</a><p>3) B-cell depletion reactivates B lymphopoiesis in the BM and rejuvenates the B lineage in aging<p><a href="http://dx.doi.org/10.1182/blood-2010-09-307983" rel="nofollow">http://dx.doi.org/10.1182/blood-2010-09-307983</a><p>----<p>Then for treatment of autoimmune disorders such as MS, more comprehensive destruction:<p><a href="http://www.eurekalert.org/pub_releases/2009-01/nu-sct012909.php" rel="nofollow">http://www.eurekalert.org/pub_releases/2009-01/nu-sct012909....</a><p>This was also tried for rheumatoid arthritis with mixed results before the development of biologics, and everyone gave up on the immune reboot with chemotherapy in favor of controlling the condition for some patients.<p>----<p>Then there are the prospects for destroying T cells specialized to herpesviruses like CMV (you probably have CMV, near everyone has CMV by time old age rolls around, it's very prevalent) that are thought to cause a large degree of immunosenescence by overloading the repertoire of immune cells with memory T cells for CMV and the like - too many of those and not enough naive T cells to deal with new threats and cancer surveillance. That isn't a going concern yet, but it certainly could be soon.