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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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