Ramifications Of Jamie Cunliffe's "morphostasis"

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Nov 21, 2015
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What are the meanings of his interpretation of the immune system?

Successful surveillance within the cell leads, where appropriate, to apoptosis
and elective suicide. This mechanism deals with most sick cells. When cells die
by necrosis, controlled shutdown has failed to protect the ZDC. Now, membranes
rupture, their contents are spilled and this promotes inflammation. Inflammation
provokes aggressive T-cell responses. When cells rupture, they release a
characteristic set of cytokines, particularly eicosanoids. These are the
messengers that notify adjacent somatic and inflammatory cells that an
uncontrolled catastrophe has occurred. Tc cells are primed to encourage cells to
enter apoptosis if they carry markers resembling cells from areas where
catastrophic death was previously encountered. Th1 cells remember the
inflammatory context in which they first met their epitope. When they
reencounter similar peptides they can then turn up the inflammatory "heat". They
do not, themselves, kill: this is left to "angrified" phagocytes that become
more particular about what they accept as HS identity. In contrast, peptide
debris processed after the phagocytosis of apoptotic cells promotes T-cell
suppression. For instance, when a cell dies following a virus infection its
debris is processed by adjacent cells and phagocytes. If cell death has occurred
following successful internal surveillance (apoptosis), tolerance will be
promoted to any presented peptide debris, including viral peptide. When
unsuccessful (eg, lytic or necrotic death), inflammation will promote T-cell
aggression to presented peptides, including self peptides. However, since
apoptosis is such a common process, most self peptides have previously promoted
suppression and so shrunk the populations of precursor T-cells capable of being
recruited into aggression against self. Furthermore, the threshold at which
uncommitted T-cells are triggered into aggression falls as they age. This helps
to focus aggression onto strange rather than common epitopes.



HS cells in an inflammatory area are relatively immune from self attack because
they still demonstrate HS identity. I contend that this is the real horror
autotoxicus. Phagocytes from closely related species share a similar
specificity. Non-pathogenic organisms are easily identified as non-self. Unless
complement is present, bacteria and viruses must rupture a cell and/or disrupt
its ICJs to invoke an inflammatory reaction and trigger an anamnestic immune
response. Many dedicated pathogens appear to have evolved mechanisms to heighten
inflammation in order to create themselves the niche they need to survive (eg,
TB).



Inflammatory cells need to be restrained from entering healthy tissues until
things go wrong since their intrusion disrupts tissue function. The endothelial
cell linings of blood vessels tend to lock out phagocytes until they are invited
in. This is done most rigorously in the central nervous system - the blood brain
barrier. This barrier is necessary as nervous function relies on the electrical
(GJ) disconnection of neurons at their terminal differentiation. The resulting
(functional) asynchronisation then makes them more susceptible to macrophage
attack (note how traumatic paraplegia is ameliorated with steroids). The need
for segregation is likely to be an important factor in the origin of the
vascular system and of inflammatory regulation...
 

LeVere

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Joined
Dec 1, 2016
Messages
49
I like him, he's a handy person to bring up when you are critiquing various germ theory ideology. If you reject the primacy of pathogenic germs then the existence of an immune system makes no sense. He also connects very well with a view that rejects the existence of viruses(exogenous viral pathogens). I'd love to see him spawn a successor or two to shake up the germ theory dominated microbiological landscape.
 

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