Further notes about the morphostasis concept – split files

(16) Assumed purpose of the adaptive immune system

Almost "to a man" articles consider the purpose of T-cells, B-cells and antibodies to be the specific recognisers of pathogenic agents (usually microorganisms of one sort or another – commonly referred to as "pathogens"). However, the evolutionary emergence of the adaptive immune system was likely (I would say certainly – 99% surity for me) to be for the memorising of patterns of excessively stressed tissues and, in particular, to act as a memory for inflammatory responses (provoked by pathogenic stimuli). Now, whilst individual epitope/paratope interactions are the final "quantal" components that add up to provoke this response (specific micro-organismal antigens are favoured because they were associated with the pathogenic stimulus) it is very likely that the system is geared to respond, most vigorously' to a pattern of epitope association rather than to individual epitopes on their own. So – and this is a very testable point – a characteristic pattern of different epitopes will reveal the re-occurrence of a previously encountered pathological stimulus. We should be able to take a pathological stimulus, analyse the epitopes (and immune response class) that lead to inflammatory amplification then provoke an animal immune response to one, then two, then three (and etc) of these epitopes and then measure the levels of the response. I would like to think that the progressive recruitment of an expanding paratopic repertoire will escalate the response – perhaps exponentially. Not all of these epitopes will be restricted to micro-organismal epitopes. Many of them will also characterise the associated self tissue damage. We already know that the immune response often retains a memory of the tissue location. It is like telling the police about a crime. "It was a robbery, a small disorganised gang were involved. They carried out the crime by breaking into the back of the building that was a small post office." Various other characteristics of the event and a description of various characteristics of the individuals who carried out the attack are noted. The police then compile a dossier of the event, look for patterns and can respond much more effectively at any repetition of a similar crime. Current "just-splat-the-bug" perceptions are very much biased towards a "one organism / one epitope" perspective and, particularly, do not differentiate a pathogenic from an incidental/commensal encounter.

One more point to emphasise is that "kill-the-bug" (splat-the-bug) perspectives ignore the feature that, I believe, is nearest to a "purpose" of the system. A bit of "me" (the zygote derived conlony) was damaged in a previous encounter. I will be on the alert for a similar future event and do what I can to limit any damage and encourage a rapid resolution to reasonable function if it does occur.

This is a useful section in which to add comments on "the latest perspectives". [Added 11/03/2023]

I have just managed to (briefly) see the latest version Janeway’s Immunobiology. This is the opening paragraph:–

“Immunology is the study of the body’s defence against infection. We are continually exposed to microorganisms, many of which cause disease, and yet become ill only rarely. How does the body defend itself? When infection does occur, how does the body eliminate the invader and cure itself? And why do we develop long lasting immunity to many infectious diseases encountered once and overcome? These are the questions addressed by immunology, which we study to understand our body's defences against infection at the cellular and molecular levels.”

The intensity and absoluteness with which they regard immunity as “a defence mechanism against infective agents” (full stop) speaks volumes about the way that even the most up to date immunology textbook takes a blinkered stance.

According to the index, this is the only mention of ElieMetchnikoff:–

“Macrophages can phagocytose pathogens and produce the respiratory burst immediately upon encountering an infecting microorganism, and this can be sufficient to prevent an infection from becoming established. In the 19th century, the immunologist Elie Metchnikoff believed that the innate response of macrophages encompassed all host defences; indeed, invertebrates such as the sea star that he was studying rely entirely on innate immunity to overcome infection. Although this is not the case in humans and other vertebrates, the innate response of macrophages still provides an important frontline of defence that must be overcome if a microorganism is to establish an infection that can be passed on to a new host.”

Again, this speaks volumes on the distorting emphasis that this obsession with adaptive immunity has inflicted on a large cohort of immunologists. The innate immune system is dismissed as an evolutionary relic, a redundant backwater that is largely usurped by the arrival of adaptive immunity.

“A unique feature of the adaptive immune system is that it is capable of generating immunological memory, so that having been exposed once to an infectious agent, a person will make an immediate and stronger response against any subsequent exposure to it; that is, the individual will have protective immunity against it. Finding ways of generating long-lasting immunity to pathogens that do not naturally provoke it is one of the greatest challenges facing immunologist today.”

This last paragraph should be read bearing in mind that the adaptive immune system probably “memorises” unique patterns of the pathogenic stimulus, not the “pathogen” (a term they regard as being synonymous with a “pathogenic micro-organism”).

Lastly, there is only a short section on the origins of immunity – the phylogeny of immununity ("The origins of vertebrate immune cells"). Hhhmmm … ??? Surely, this is where we should find big clues on what it is really all about, do you not agree?