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represents a very important and fundamental mechanism of regeneration of immu-
nocompetence during recovery from severe illness. During acute illness, the ADIM
system is suppressed due to amplification of the NATIM system by CTKs, GCs, and
CATs. This occurs in the majority of individuals who do not age successfully and
succumb to various illnesses that activate the NATIM and suppress ADIM. The pro-
longed activation of NATIM may lead to extreme weight loss ( cachexia ) and eventu-
ally death [26] .
The concept of age-related immune deficiency led to doom-and-gloom prospects
concerning aging. However, successful aging, without disease, has been observed.
Therefore, at this time it is clear that disease-free survival is possible until we reach
the natural limit of our lifespan [124] .
1.7 Conclusions
Proposals of neuroimmune interaction date back to the late nineteenth century. The
students and followers of Pavlov studied neuroimmune regulation in Russia and con-
cluded that the hypothalamus was involved as a central immunoregulatory organ.
Andor Szentivanyi (1950-51) demonstrated first with objective methodology that the
hypothalamus regulates the anaphylactic reaction and antibody formation in labora-
tory rodents. Korneva and Khai [7] confirmed that antibody formation is regulated by
the hypothalamus. Ader [16] and Gorczynski and Kennedy [17] showed that immune
reactions are sensitive to Pavlovian conditioning.
Hans Selye described the stress syndrome [8], which was characterized by the
activation of the HPA axis and the involution of the thymus and lymphoid organs. He
pointed out that stress leads to the “general adaptation syndrome,” which protected
the animals from “nocuous” agents.
This early scientific inquiry progressed slowly, with only a few laboratories work-
ing on this field. Neither the immune nor the neuroendocrine systems were known
well enough to permit a detailed analysis of neuorimmune interactions. The situation
changed gradually during the mid-1970s when pituitary hormones were studied for
immunoregulation. It was discovered that GH and PRL stimulate ADIM function,
whereas the HPA axis was shown to have immunosuppressive and anti-inflammatory
effect. The initial papers on the subject were followed by investigations in numerous
laboratories and the fundamental nature of neuroimmune interaction has been elic-
ited. It was shown that the HPA axis is stimulated by IL-1, a CTK produced within
the IS. Soon other pituitary hormones and numerous (type I) CTKs were found to be
involved in “feedback” communication of the IS with the neuroendocrine system.
It appears that in utero the IS relies on placental lactogens for development. After
birth, pituitary GH, PRL, IGF-1, and the HPA axis are involved in regulating ADIM
function. This applies to naïve lymphocytes. After priming with antigen, ADIM cells
depend on type I CTKs for their survival and function. This is the case also for mem-
ory cells. Type I CTKs also support the HP and survival of naïve and memory T cells,
B cells, and NK cells. However, in situations when CTKs are in short supply, such
as severe radiation disease for instance, and a number of other “stressful” conditions,
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