Further notes about the morphostasis concept – split files

(20) Oddments

• The adaptive (anamnestic) immune system does NOT discriminate self from non-self.
• Self non-self discrimination DOES occur and is carried out in and by all cells on the basis of ligand receptor interaction of WHOLE cells. "Non-self" includes unhealthy self cells. So, it is healthy-self-cell/other-than-healthy-self-cell discrimination.
• Self epitopes (loosely – antigens) are NOT part of or the basis of a "horror autotoxicus" principle. Self reactivity is ALLOWED and may be triggered into aggression. However, the massive apoptosis of effete self cells that occurs both in the thymus and all over the body – every day – favours the promotion of immunological tolerance to self epitopes. But this does NOT result in the rigid observation of tolerance to these self epitopes.
• For my money, "danger" is far from an ideal metaphor. "Damage" would be better. The anamnestic immune system is largely preoccupied in categorising cellular debris into well packaged debris (successful controlled cellular shutdown – largely apoptotic debris) and spilt cellular debris (messy death). This categorisation allows the system to leave the successful inner shells of the immune system to get on with another successful job when a similar incident is reencountered. It also ramps up the inflammatory process on re-encountering characteristic messy-death-debris. This gives inflammation a memory (a poorly emphasised tautology).
• The evolutionarily older innate immune response is dominated by an inflammatory ingress of phagocytes. In invertebrates, this response is not dependant on adaptive immunity. In vertebrates, the initiation of an inflammatory (phagocyte led) response has been substantially isolated from its execution; the adaptive immune system now bridges this divide and is able to greatly amplify the inflammatory response. Dampening inflammation is desirable in the eye and the brain. An intense amplification of inflammation by the adaptive immune system would be most unwelcome here.
• It is generally assumed that the adaptive immune system responds with equal force to epitopes for which it has developed paratopes (antibodies or T-cell receptors). However, if we assume that the system is remembering not a "pathogen" epitope but a signature of damaged tissues (a pathogenic stimulus) then it is probably a safe bet to assume that a "memorised" pathogenic stimulus is composed of a pattern (or system) of epitopes. On re-encounter, the level to which inflammation is amplified is probably going to rise (perhaps exponentially) with the progressive recruitment of more and more identifying paratopes that were used to take a snapshot of this earlier encounter with a "pathogenic stimulus". So, rather like pinning a crime on a suspect, the certainty of identification rises as the number of different identifying features and evidences coincide. I think that this is a very likely scenario that could be investigated to be confirmed or negated.
• Evolution – can take large phenotypic jumps that are associated with small genotypic jumps. Large genotypic jumps are probably confined to translocations and deletions (chancy rearrangements).
• Entropic saturation only applies to a closed system. Where there is entropic flow, then this is the outcome of the connection of previously separated systems.