Biology Reference
In-Depth Information
T lymphocytes within the ADIM system. The related dendritic cells are regarded as
“professional” antigen-presenting cells of the ADIM system. Monocytes recirculate
in the blood and macrophages are distributed in tissues throughout the entire host
organism. These phagocytic cells recognize infections and other noxious agents
through their INIRs, engulf the microbe/foreign material, digest (process) it, and
present peptides via their major histocompatibility-II (MHC-II) surface antigens to
T lymphocytes of the ADIM system. This is the
phagocytic pathway
of antigen
presentation. Therefore, monocyte-macrophage activation within the INIM system
almost inevitably activates T cells of the ADIM system, so that the entire NISS is
mobilized to fight the intruding pathogen/noxious agent. This conclusion is further
supported by the fact that
all nucleated cells
are capable of presenting cytosolic anti-
gen via their surface MHC-I to T cells
[20-22]
.
Once the ADIM system is activated, cytotoxic and helper effector T cells are
produced. As a rule, antibody formation also follows after B lymphocytes present
antigen to helper T cells and such T cells stimulate B lymphocytes to form antibod-
ies. Immunoglobulins D (IgD) and M (IgM) are formed as surface immunoglobulins
by B cells. After an immune response, IgM is secreted first, and later the same B cell
may switch to making IgG, IgA, or IgE, depending on the regulatory environment of
the cell. All the different classes of antibodies made by one B cell are specific for a
single epitope of the antigen to which the cell was responding
[21,22]
.
IgM, IgG, and IgA are able to fix complement after combining with the antigen.
Complement
is an enzyme system belonging to the INIM system. Moreover, all leuko-
cytes express receptors for fraction C (Fc) the binding of antibodies to their surface, and
use such antibodies for better identification of pathogens/noxious agents. Here INIM cells
use ADIM antibodies. The complement system has three pathways for activation: by
Figure 1.1 (cont.)
The primary immune response is dependent on pituitary PRL and GH. These pituitary
hormones regulate cell growth throughout the entire organism according to this principle.
IGF-1 acts like a second messenger in most situations. The HPA axis inhibits ADIM and
stimulates NATIM. CATs support the immunoregulating activity of the HPA axis.
Type I CTKs produced within the IS will gradually take over the role of PRL/GH, and the
secondary response gradually becomes independent of pituitary hormones. Memory T cells,
B lymphocytes, and NK cells survive severe illnesses by HP and regenerate immune function
during healing. The hypothalamic hormone VP stimulates PRL and the HPA axis and thereby
regulates the process of healing, and maintains ADIM and NATIM in homeostatic harmony.
This figure illustrates that the entire host organism communicates and cooperates with the
central regulatory network. Innervation, hormones, CTKs, chemokines, and recirculating
leukocytes serve as communication pathways. These pathways of communication are
open at all times. No immune response, inflammation, or infection can occur in any tissue/
organ in the body without signaling the hypothalamus, PVN about such events. Therefore,
infection, inflammation, and immune reactions are under continuous surveillance within the
NISS. During homeostasis, this system protects us very efficiently, without disturbing any
physiological functions in the body.
Source:
Adapted from Ref.
[124]
.
