Further notes about the morphostasis concept – split files

(41) And still more on "pathogens"

Science has just presented an article in which it says this, "Human skin, the body's largest organ, functions as a physical barrier to bar the entry of foreign pathogens, while concomitantly providing a home to myriad commensals." (The emphasis is entirely mine.) So what is a "foreign pathogen"? This seems to me to be a strange mish-mash of confused perceptions. It encompasses "the skin (and immune system?) responds to foreigners"; it encompasses "pathogens are microbes"; it seems to imply that "commensals are not foreigners" (or for that matter capable of being pathogens). To me, this simple phrase immediately confuses the issue of what is really happening.

This all points back to the point, "Show me how the cellular adaptive immune system (vs antibodies) directly attacks micro-organisms (M-Os)." My challenge is that you cannot. It can encourage (self) cells (displaying a peptide/Mhc_Class_I signature that was created from the debris of a M-O) to go into premature apoptosis. It can amplify an inflammatory reaction in the vicinity of a peptide/Mhc_Class_II signature and this makes life uncomfortable for proximal M-Os. However, there is NO direct attack on the M-O. Antibodies, also, tend to prepare their target for enhanced inflammatory (phagocytic) clearance. The only exception is where a M-O may be sickened by strong C8/C9 complement deposition on its membrane. They can also disable the M-O's pathogenic mechanism to make the M-O impotent in attack. Otherwise, the antibody/complement interaction opsonises the M-O ready for inflammatory (phagocytic) attack. Why do immunologists persist in insisting that the M-O is directly attacked by adaptive immunity? Without an inflammatory effector mechanism, the adaptive immune system is impotent (even apoptosis encouraged by Tc cells needs phagocytic clearance).