Biology Reference
In-Depth Information
PRL is neutralized by antibodies, the rats develop rapid wasting, immunodeficiency,
and bone marrow failure and die within 6 weeks
[57]
. Congenital lack of the pituitary
gland is lethal
[58]
. Lymphocytes are capable of synthesizing GLHs. The lymphocyte
PRL gene is associated with the pituitary-independent placental promoter
[59,60]
.
T lymphocytes secrete PRL into the rheumatoid fluid, which stimulates inflammation
[61]
. Type I cytokines and GLHs share the JAK-STAT signal transduction pathway
[62]
. The differentiation of innate immune B lymphocyte is regulated by estradiol,
and the differentiation of adaptive immune B lymphocytes is regulated by PRL
[63]
.
In this context, it is important to keep in mind that both the immune and neuroendo-
crine systems are redundant systems and in case of the destruction of one pathway
several others may be available to substitute for the function lost.
7.4 Sensing and Regulating Inflammation: Mast Cells
as Sensory and Neuroeffector Cells
Tissue mast cells have long been regarded as inflammatory cells that store numerous
inflammatory mediators and discharge them in response to various noxious stimuli,
thereby causing inflammation
[64]
. More recently, it has become clear that mast cells
are integrated into the immune system by binding IgE antibodies to their surface
Fc-epsilon receptors (Fc,R). After the specific antigen (allergen) meets its antibod-
ies on the surface of mast cells, the mast cells discharge their contents and a rap-
idly developing inflammatory response follows (immediate hypersensitivity)
[65]
. At
present, IgE-mediated hypersensitivity is accepted in mainstream immunology as the
cause of allergy, and major efforts are being undertaken to inhibit the IgE response
on the assumption that without the antibody, allergy will not develop. However, it is
well known that asthma may also be of IgE-mediated (allergic) origin, though there
is a nonimmune, “idiopathic” form of this disease
[66]
.
7.4.1 Mast Cells as Sensory Cells
Mast cells are innervated (
Figure 7.1
)
[67,68]
and mediate neurogenic inflammation,
which is a major effector arm of the neuroimmune supersystem
[3,24]
. Therefore,
mast cells serve as nociceptors, immunologically specific receptors capable of deliv-
ering information to the CNS about approximately 10
11
epitopes. Mast cells also
recognize complement split products (C3a, C5a;
anaphylatoxins
)
[2]
and inform
the brain about complement (C) fixation, in addition to causing inflammation in
response to C activation. Bradykinin is an inflammatory mediator that signals the
brain about inflammatory events via sensory nerves
[24,69]
.
7.4.2 Mast Cells as Neuroeffector Cells: Neurogenic Inflammation
The sensory nerves that innervate mast cells come from the dorsal route of the spi-
nal cord, but sensory fibers are also present in the vagus nerve. The neuropeptides,
substance P, calcitonin gene-related peptide, and neurokinins A and B (tachykinins)
