Biology Reference
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is largely, but not entirely, concerned with immunogenic agents. Here antigenic
receptors dominate. This system is also subject to conditioning. Therefore, the acti-
vation of the INIM system, with or without adaptive immunity, is responsible for the
profound host resistance to diverse noxious agents. The NISS is capable of mobi-
lizing the entire organism in the interest of host defense in emergency situations
(through APR). The same NISS performs important physiological functions, as is
becoming apparent with further research [53,54] .
1.3.1 Hierarchy in Regulation
The regulatory portion of the NISS consists of hierarchical regulatory circuits , which
are superimposed on each other. For example, regulatory signals from a higher cir-
cuit (such as the CNS) are capable of dominating the signals from lower circuits (e.g.,
pituitary). As we know, pituitary hormones control hormones secreted by the adrenals,
gonads, thyroid, liver, and other tissues that secrete insulin-like growth factor (IGF).
CTKs, which are tissue hormones, represent another regulatory circuit. Our experiments
indicate that if a higher regulatory circuit fails, a lower circuit will gain dominance and
take precedence over lesser signals that still exist in the system; this way, INIM function
is maintained continuously under any circumstance [63] . This means that the INIM
system continues CTK production during acute illness/injury under any conditions, and
these CTKs will signal any regulatory circuits of the host organism that remain active.
Hence, the INIM system never stops protecting the host organism ( Figure 1.2 ).
Figure 1.2 (cont.)
hormones, represent another regulatory circuit. If a higher regulatory circuit fails, a lower
circuit will be stimulated via INIRs or by CTKs and thus will continue to regulate the lesser
circuits that still exist in the system. INIM function is maintained continuously under any
circumstances [65] . CTK production continues during acute illness/injury through the INIM
system. The INIM cells are capable of performing on their own if necessary; the INIM system
never stops protecting the host organism.
INIRs are present throughout the entire organism. Therefore, when infectious/noxious
agents are contacted, every regulatory circuit is capable of activating a response independent of
the other circuits if necessary. For instance, LPS (which activates TLR4) stimulated ACTH and
GC secretion in PVN-lesioned rats [67] . LPS also stimulated natural antibody formation in B
lymphocytes, and is able to stimulate many other systems in the body, including the CNS [22] .
Abbreviations to Figures 1.1 and 1.2.
ACTH  adrenocorticotropic hormone, ADIM  adaptive immune, ALD  aldosterone,
APP  acute phase proteins, CAT  catecholamines, CTK  cytokine, CRH  corticotropin
releasing hormone, GC  glucocorticoids, GH  growth hormone, GMCSF  granulocyte-
macrophage colony stimulating factor, HP  homeostatic proliferation, HPA  hypothalamus-
pituitary-adrenal axis, IGF-1  insulin-like growth factor 1, IL  interleukin, INIM  innate
immunity, INIR innate immune receptor, INS  insulin, PVN  paraventricular nucleus,
PRL  prolactin, NATIM  natural immunity, SH  steroid hormone, MHC-II  major
histocompatibility complex-II, NGF  nerve growth factor, NK  natural killer,
NPEP  neuropeptide, TNF  tumor necrosis factor, T4  thyroxin, Tsr  suppressor/
regulatory T cells, TSH  thyroid stimulating hormone, VD3  vitamin D3,
VP  vasopressin.
 
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