Can you translate your terms into those used in immunology ?
I'm guessing by 'adaptive' you mean humoral, but I have no idea what 'innate' means.
Both our innate immune system (using genetically coded Pattern Recognition Receptor systems (like TLR (Toll like receptors), NOD receptor, and RIG receptors, and cytosolic DNA sensors – all of which evolution tuned an exquisitely to the DNA, lipid and glycoprotein signatures of various pathogens), on the one hand and adaptive immunity, on the other hand, using antibodies and other forms of learned tagging of pathogens) have both what we traditionally think of cellular and humoral (blood-born) aspects. TLR lead directly via an fairly standard chain of signals/interactions to immediate production of cytokines. No learning is needed.
Adaptive immune system requires a mediating 'handoff' from class of macrophages referred to as dendritic cells which present antigens to T cells which in turn act sometimes as generals but also as foot soldiers so to speak in the adaptive immunity process. T cells promote B cells, which ramp up antibody production. (See graphic below)
Aging is relevant into this as it appears to reflect a disinhibition of the innate immune system as a partial but ultimately not very adaptive compensation for the age-related down regulation of adaptive immunity, which is multifactorial but principally a decline in naïve T cells which means that the system is a sluggish learner. If you pair that with a dis-inhibition of the inflammatory process that is intrinsically tied to innate immunity And that is less targeted and capable of destroying our own tissues en mass, I believe you may have an explanation for why a higher percentage of folks die from this disease who are older. They have a poorer transition from innate to adaptive immunity, a disinhibited and more destructive pro-inflammatory response, and if you consider that many so-called 'comorbid' conditions are actually themselves associated with upregulated systemic inflammatory signals (For sure heart disease, cancer, and type II diabetes at a bare minimum). These conditions may index poor regulation of what you might call the 'background tone' in the Innate immune system (Metaphorically it's kind of like having your senile fire department go out and break down doors and hose down houses
just in case there might be a fire there), I believe you begin to approach an explanation for the differential mortality of Covid 19. This is just one person's moderately informed speculation.
I came by these concepts as an Alzheimer's disease clinician for 30+ years, during which time i was also a chronic research consumer and reviewer, and editor for
Frontiers in Aging Neuroscience. This problem (referred to as "inflammaging" by an Italian researcher) may clarify at least some dimensions of significant risk for AD. It took me years to undo the damage early in my training associated with the most unfortunate concept of the brain as "an immune privileged site". Never quite understood how the most important organ in the whole system was "immune-privileged," but I didn't have enough confidence in my skepticism when I was in training in the early 80s to say "no way that made any sense." I've since learned to listen to my skepticism better.
The
Wikipedia entry on the immune system is not bad as a overall summary around these issues, although it mixes up a few things.But I recommend it to folks who want a mid-level semi technical treatment of these issues.
Hope that's helpful.
