Further notes about the morphostasis concept – split files

(46) Innate immune memory

This month's Nature Immunology (August 2015) has an article on "Innate immune memory: a paradigm shift in understanding host defense" . This commentary presents some clues as to why the obvious may have been missed; the obvious, here, being that the adaptive immune system acts as a memory for past inflammatory encounters, rather than it being a system that memorises invading (micro–)organisms (generally referred to as "pathogens" but what I prefer to call "pathogerms").

They state: "The consensus until recently was that [innate immune cells] mount nonspecific responses and they are not able to confer immunological memory on their own. In contrast, the adaptive T cell– or B cell–dependent immune responses are antigen specific and they often provide lifelong protection against re–infection." Implicit in this statement is the continuing assumption that adaptive immunity targets and attacks micro–organisms ("pathogens") directly. It ignores the point that it is damage–associated–then–processed–debris that initiates aggressive immune responses. If the "debris" is dominantly from apoptotic bodies (with some excess of panic [damage] signalling) then Class I (CD8) responses are invoked. If it is dominantly phagocyte–ingested–spilt–cytoplasmic–debris, then Class II (CD4) responses are invoked. The effect of the CD8 response is to encourage an expeditious apoptosis of similarly tagged self cells. The effect of CD4 responses is to ramp up the innate immune response (inflammation) in the vicinity of phagocytes that display processed and memorised peptide fragments on the cell exterior, within the peptide grooves of Class II Mhc molecules. What is recognised is self phagocytes displaying (phagocyte) processed debris that the phagocyte had earlier ingested as debris and that was associated with spilt and damaged cytoplasmic contents.

Note that the free antibody response (plasma cell derived circulating antibodies) is more complex and more apparently a direct attack on "pathogens" ("pathogerms"). However, for all but IgM responses, the licencing of plasma cells (to produce antibody) involves CD4/B-cell co-operation and is similarly restricted to peptide–in–self–Mhc–class–II presentation.

I can only access the first page of this article so I do not know if they have addressed this aspect of adaptive immunity (a memory for pathogenic events – assuming that the word pathogen means any damaging agent whether biotic or abiotic). However, I suspect, from the abstract and introduction, that this is not discussed.