Further notes about the morphostasis concept – split files

(50) Our immune system evolved to . . . .

These are typical and extant statements:

• – attack foreign materials entering our body
• – fight infections so we could survive and pass our genes to the next generation
• – protect us from the danger that lurks with invading micro-organisms such as bacteria or viruses
• – protect us against the attack of foreign microorganisms
• – only fight one enemy, bacteria
• – fight infectious diseases
• – handle and control a number of different pathogens
• – cope with a constant onslaught of opportunistic microbes
• – recognize pathogenic microorganisms and to react to them with a powerful, destructive response
• – protect us from a germ-laden world

I am going to suggest a rewording that makes things clearer – I think.

• – our adaptive immune system evolved as a debris classification system.

This debris has been processed within a cell and broken down into short peptides. It is processed either in the cytoplasm of any cell (Class I / CD8 processing) or within the phagosomes of an antigen presenting cell (Class II / CD4 processing). These peptides are displayed on the cell surface attached to self Mhc molecules. The appropriate T-cell receptor recognises these Mhc/peptide complexes NOT as "pathogens" (micro–organisms) but as self cells, identified by self Mhc, subtly modified to act rather like an allo–Mhc ligand (altered self). The "pathogen" (micro–organism) is never recognised by T–cells in its native state; what is recognised is the debris that its earlier demise has generated within a cell. This cell has (necessarily) broken down the organism and "trashed it" into short peptides to display these (in an Mhc groove), on the cell membrane, as a signature of the internal "turmoil" that it is experiencing. The micro–organism must have already died and been disposed of for it to have rendered this peptide available for loading into the Mhc groove. Naive T–cells that interact with an appropriately specific Mhc/peptide (which can now be regarded as an epitope) can be committed to tolerance or aggression. This is done according to the usual inflammatory/non-inflammatory milieu in which this epitope is encountered so that this milieu can be rapidly exaggerated on reencounter. To repeat, this debris is recognised by T-lymphocytes but only as processed peptides resting in the peptide groove of Mhc molecules. This means that the parent protein has already been processed and degraded within a cell then "hung out" for display. It is not the parent protein that is recognised; it is the processed protein – broken down to a peptide – that is recognised. All subsequent "actions" either lead to an exaggerated reproduction of the inflammatory/non-inflammatory milieu typical of its triggering encounter (T_h effector/Class II presentation) or encourages the tagged cell into a premature apoptosis (T_c effector/Class I presentation). Effectively, this provides the "debis response"/"inflammatory process" with a memory. T–cells DO NOT recognise and interact with the native "pathogens" (micro–organisms). They do not kill "pathogens" though they do encourage an environmental response that encourages an exaggerated/facilitated innate response to their presence. This innate response includes elective suicide (apoptosis/programmed cell death) acting as an inner defence barrage to phagocytosis (see the "Phlogiston" article).