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Tolerance is a fundamental property of the immune
system.
Tolerance involves non-self discrimination which is the
ability of the normal immune
system to recognize and respond to foreign
antigens, but not
self.
Autoimmunity is evoked when this tolerance to self antigen is
broken.
Immunological
tolerance within an individual normally begins as a fetus.
In
maternal fetal tolerance T cells express receptors specific for a specific
antigen enters the circulation of the developing fetus via the
placenta.
Fetal T cells orginate in the bone marrow where they begin
growth but must travel to thymus where maturation of T cells
occurs.
Within the thymus fetal T cells encounter various self and
foreign antigens.
In this manner T cells, attenuated to pathogens,
become pathogen hunters.
Approximately 99 percent of fetal T cells die
through induction of apoptosis in the thymus in the attempt to convert T cells
into pathogen hunters.
An autoimmune response
can be incited through molecular mimicry.
Molecular mimicry involves
the ability of similar molecular structures from dissimilar genes or proteins
to mimic similar organic self structures.
Dissimilar sequence partial
structures may elicite an autoimmune response.
Virulent proteins,
through molecular surfaces, can mimic host protein surfaces.
Through
molecular mimicry a pathogen can generate autoimmunity.
The pathogen may mimic
either the linear amino acid sequence or the conformational fit of the
immunodominant epitope.
An
autoimmune response is then generated by any similar pathogen.
Pathogens alter macrophage function, act as
mutagens and
cause the release of cytokines.
Due to similar sequence homology in the
immunodominant epitope between the pathogen and the host, cells and tissues of
the host associated with the protein are hunted down as a result of the
autoimmune
response.
Findings from biological research suggest that sustained
involvement in gratifying activities
such as the creation of works of art or walking through Ponderosa pine
forests result in positive immune system
responses.
The protective effect of cannabidiol (CBD), the
non-psychoactive element of Cannabis sativa, against neuronal toxicity induced
by cadmium chloride (CdCl2 10 µM) was investigated in a retinoic acid
(RA)-differentiated SH-SY5Y neuroblastoma cell line. These data showed that
Cd-induced neuronal injury was ameliorated by CBD treatment and it was
concluded that CBD may represent a potential option to protect neuronal cells
from the detrimental effects of Cd toxicity.
Cannabinoids protect neurons from excitotoxic
injury. We investigated the mechanisms involved by studying
N-methyl-d-aspartate (NMDA) toxicity in cultured murine cerebrocortical neurons
in vitro and mouse cerebral cortex in vivo. Cannabinoids seem to protect
neurons against NMDA toxicity at least in part by activation of CB1R and
downstream inhibition of PKA signaling and NO generation.
Cannabinoid receptor agonists act presynaptically to
inhibit glutamate release. The effect of prolonged drug exposure on the
neuroprotection afforded by cannabinoid receptor agonists was also studied.
Desensitization of CB(1) receptors diminishes the neuroprotective effects of
cannabinoids. This study demonstrates the importance of agonist efficacy and
the duration of treatment on the neuroprotective effects of cannabinoids.
In summary, we have shown that in an in vivo model
of neurodegeneration Δ9-THC reduces neuronal damage via a
CB1-receptor-mediated mechanism. This holds in both the acute and late phase
after induction of excitotoxicity. Δ9-THC inhibits astrogliosis
via a non-CB1-receptor-controlled mechanism. The results strengthen the concept
that the endogenous cannabinoid system may serve to establish a defense system
for the brain. This system may be functional in several neurodegenerative
diseases in which excitotoxicity is thought to play a role, such as amyotrophic
lateral sclerosis, Huntington's and Parkinson's diseases, and also
in acute neuronal damage as found
in stroke and traumatic brain injury. It is conceivable that the endogenous
cannabinoid system can be exploited for therapeutic interventions in these
types of primarily incurable diseases. |
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