Revival: Biological Effects of Low Level Exposures to Chemical and Radiation (1992)

EFFECTS ON IMMUNE RESPONSE 109

Figure 5.12. Influence of irradiation upon primed versus unprimed cells. Mice were
injected with SRBCs or saline 40 days prior to sacrifice. Spleen cell
suspensions were exposed to indicated doses of radiation in vitro and
placed in 1-mL cultures. Results expressed as a percentage of the control
response. Adapted from Anderson and Lefkovits.16

injury initiates the “apoptotic pathway” at a point subsequent to the initiat­

ing intrathymic event. Thus, it is entirely a chance phenomenon that the

end result is the same.

2. Competitive advantage. Since all forms of life are continuously exposed to
   various forms of “natural” or background radiation, perhaps low-dose
   exposure offers a competitive advantage via nonspecific augmentation of
   the immune response. The resting state, according to this line of thinking,
   is really not resting but rather one of heightened reactivity as a conse­
   quence of background exposures. This proposition seems unlikely, espe­
   cially since the doses associated with augmentation experimentally are sev­
   eral logs larger than those experienced from natural exposures in most
   parts of the world.


3. Curb against autoimmunity. It is clear that the mammalian host goes to
   great lengths to protect itself against autoreactive lymphocytes. In particu­
   lar, the passage of pre-T cells through the thymus is accompanied by the
   loss of most of these cells, presumably to protect the host against the
   release and peripheralization of cells with self-reactive potential. In this
   context, it is important to note that the lymphocyte is the only mammalian
   cell that can undergo extensive clonal expansion postnatally. As a conse­
   quence, one renegade autoreactive lymphocyte could in theory proliferate
   in response to histoincompatible host antigens, thereby developing a self-
   reactive clone capable of killing the host. Similarly, a lymphocyte that is
   injured but not killed by irradiation poses a distinct threat to the host,
   especially if the damage involves the nucleus. Nonlethal damage to lym­
   phocyte DNA could result in the mutation of genes associated with regula-