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antigen-antibody complexes (ADIM, classical pathway); by microbes (INIM, alternative
pathway); and by lectins (INIM) [21,22] .
We proposed that the Tsrs is a member of the innate INIM. The evidence comes
from the activation of Tsrs by CATs and GCs. These hormones activate INIM cells
and suppress ADIM cells [31] . During severe trauma or infectious disease, APR
develops whereby ADIM is suppressed and the INIM system takes over command
for the highly coordinated and very intensive immunological battle to save the host
organism [26-28] . The INIM system, which is with us at birth, initiates most of the
immune responses against microbes and other noxious agents; it regulates adaptive
immunity by antigen presentation and by Tsr cells that suppress ADIM. Therefore,
the INIM system is the first to protect the host, and it continues to protect the host till
the last moment of survival [27] .
1.2.3 The Role of Innervation, Neurotransmitters,
and Neuropeptides
Lymphoid organs, such as the spleen, thymus, and bone marrow, are innervated [32] .
This fact indicates that the CNS is in permanent contact with the IS. In addition, neu-
rotransmitters and neuropeptides regulate inflammation and immunity [33] . The media-
tors involved may stimulate or inhibit immune and inflammatory processes. Substance
P, neurokinin A and B (collectively known as tachykinins ), calcitonin gene-related pep-
tide (CGRP), and vasoactive intestinal peptide (VIP) are pro-inflammatory mediators
capable of eliciting an inflammatory response. These mediators also enhance various
immune responses. In contrast, somatostatin and galanin are anti-inflammatory and
immunosuppressive mediators [31,33,34] .
Alpha-adrenergic mechanisms stimulate immunity and inflammation, whereas
beta-adrenergic mechanisms inhibit inflammation, allergy, and asthma and exert an
immunosuppressive effect. Cholinergic mechanisms are both anti-inflammatory and
immunosuppressive [35-37] .
1.2.4 Hormonal Immunoregulation
Adaptive immunity is under pituitary control. Growth and lactogenic hormones
(GLH) stimulate adaptive immunocompetence, and the HPA axis is inhibitory. The
secondary antibody response is partially independent of the pituitary. This observa-
tion suggests that memory cells are able to operate independent of pituitary hormones
[38] . GCs and CATs promote natural immunity (NATIM) and inhibit the ADIM sys-
tem by the stimulation of suppressor/regulatory T cells. Numerous other hormones,
CTKs, neurotransmitters, and peptides also modulate immune function [28] .
Innate immunity functions in the absence of the pituitary gland. From our experi-
ments, it appears that VP stimulates the INIM system, but this result remains to be
confirmed. The HPA axis exerts an important moderating effect on CTK production.
Excessive CTK production can occur after INIM stimulation if the HPA axis is not
functional (see Section 1.2.1).
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