However I am afraid, it still does not suggest that antibodies on secondary immune response can be secreted without presentation of same antigen to memory cells.
Well, at this point you're just running around in cricles. You've been given every answer you need, and seem to be floundering on your own erroneous presuppositions. If you go back and read posts
#5-9↑, you'll see we're still circling around what
Exchemist↑ calls "nonsense", and
Billvon↑ refers to as "making shit up".
So, consider, please: There is a question you're asking, but the rest of us apparently have to figure out what it is. Or, there is a question you're asking in hope of finding a particular answer, and will keep asking until someone gives it, regardless of whether or not it is true.
Think of it this way, Kumar:
You're disputing with evolution. #5, for instance, "what is the need of keeping long term antibodies for say 6 to 12 months post infection"; the answer is that organisms in our lineage fared better over time with immunological memory, and that is the trait that survives. Or #7, "if new antibodies keep on secreting yill 6 months to 12 monts, it can also be suggestive of that some traces of virus still exist in body in some dormant or accumulated state for say 6 months to 12 months"; that's not how it works. Plasma cells in bone marrow, for instance, continue making antibodies because that is what they do; it is what they exist for, and any given plasma cell will follow its programming¹ because that is what it does.
So to answer
#10↑ for instance, yes, new antibodies; and per your follow-up circling 'round at
#12↑, plasma cells in bone marrow are the example showing the process does not require a particular trigger. Which brings us to
#14↑, and the answer is that such cells will still be producing antibody
because that is what they do. And it's the same answer you get for your reiteration at
#16↑. A plasma cell in bone marrow is not going to suddenly hibernate until it receives new instructions; once programmed to its function, it will perform that function until it dies. Yet, you just keep pushing the same question, over and over.
#18↑? Same answer: If you ask, "which antigen can be there to stimulate long term antibody production even by these cells after virus infection is cured", the answer is
the original one; that is, the one that caused the plasma cell to activate in the first place.² As
Billvon↑ explained, "you need an antigen to START antibody production. You do not need an antigen to CONTINUE antibody production." Still, you just asked again in
#20↑; "how this long rerm antibody can exist without reinfection or antigen presentation", and though you were answered, you simply insisted and asked again in
#22↑, "how these long lived cells go on producing antibodies without antigens". And, again, the answer is the same as it ever was, that once those cells start, they don't stop until they die.
Second infection, unlike the first time through, might encounter existing antibody disrupting infection, and NK cells will already know what to do if they re-encounter a known antigen. Moreover, once dendritic cells present antigen at lymphoid organs, it is a quicker process to activate plasma cells and program lymphocyte affinities, because the immune system already knows this particlar antigen. This is why the secondary immune response is quicker and stronger than the primary encounter and response.
Meanwhile, per
#23↑, no, that's not how it works. The discussion about chronic illness considered the longer-term effects of immediate damage, such as pancreatic disruption resulting in the emergence of diabetes, or kidney disease related to blood clotting problems associated with Covid.
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Notes:
¹ It's in the textbook; see #29↑ above.
² Again, see #29 for the textbook excerpt.