Sorry but ,whether above quote about Memory B [Cells] suggest anywhere [that] long term antibodies can be produced and secreted without exposure of same antigen again to these cells?
My unsatisfaction is also supported by information given on many sites. Yes memory cells are created due to primary exposure of antigens either by infection or by vaccination but these are activated only after secondary exposure of same antigen and I simply want to know which is this secondary antigen?
Above site [suggest] about long term immune protection by Memory B cells. However although it is not [very] clearly indicative in it [that] re [exposure] of same Antigen is needed for long term [antibody] production but [some] [relevant] hints sre there.
Let me be clear: All of that is wrong; you keep coming back to a mystery that isn't there.
In
#52↑, you ask what about a certain quote regarding Memory cells suggests long term antibodies can be produced without new exposure to antigen; that question was already resolved. Adding in your dissatisfaction per
#54↑, that you simply want to know which is this secondary antigen, this, too, is already answered. Thus, we return to what I told you in
#47↑:
• 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.
Note the phrase,
re-encounter a known antigen. Also, observe the point that
the immune system already knows this antigen. Moreover, the paragraph considers the
secondary immune response compared to the
primary encounter and response.
Re-encounter can occur along diverse vectors. It is possible to receive a previously-encountered antigen from an external source. Presently, researchers are exploring how Covid 19 interacts with fat cells, including the question of viral reservoir (
see MacDaragh and Caplice (2020)↱), which could offer an internal source for secondary antigen exposure.
Meanwhile,
Neurath, Überla, and Ng (2021)↱:
Given the high turnover of intestinal epithelial cells persistence of the viral antigen is also suggestive of continuous virus replication. As even small amounts of persistent viral antigen have been suggested to fuel antibody evolution, the observation on persistent N protein expression over prolonged periods of time is consistent with the relative persistence of SARS-CoV-2 IgA antibodies and continued antibody evolution, as well as persistent polyfunctional SARS-CoV-2 antigen-specific B and T cell memory responses.61 These immune responses in turn are likely to support a rapid and effective adaptive immune response to the virus on re-exposure and thus provide a critical cornerstone in immune protection against COVID-19. However, one cannot exclude the possibility that long-term shedding of viruses might contribute to long-term COVID-19 and we feel that this point requires further investigation.
Part of the problem, of course, is that you keep focusing on memory cells, and in the wrong context. Your address of the
Nature article↱ is strange: You note the article "[suggests] about long term immune protection by Memory B cells", but toward your own suggestion that "it is not [very] clearly indicative … [that] re [exposure] of same Antigen is needed for long term [antibody] production", we should consider the actual relevant hints: First, the article summary below the headline explains, "People who recover from mild COVID-19 have bone-marrow cells that can churn out antibodies for decades"; this actual ongoing antibody production provides long-term protection. The article lede explains, "Many people who have been infected with SARS-CoV-2 will probably make antibodies against the virus for most of their lives", and this is because of "long-lived antibody-producing cells in the bone marrow". Memory B cells are first mentioned in the fourth paragraph, the very same sentence informs us, that "bone marrow plasma cells (BMPCs) hide away in bones, trickling out antibodies for decades".
And now,
time out. We need to circle back to
#28↑ above, when I answered your post at
#27↑, I also referred back to
#26↑, in which you compared "cash in hand or current account or kinetic energy" to the immunologic memory. And as I said,
computer code is a better analogy. And that is important, because here we are: "A plasma cell is our life history, in terms of the pathogens we’ve been exposed to", the B-cell immunologist tells
Nature. There is your computer code analogy; "memory B cells patrol the blood for reinfection", the article explains.
Moreover, both the summary and the last paragraph of that article make a particular relevant point, that "viral variants could dampen" antibody protection, noting the "ability of some emerging SARS-CoV-2 variants to blunt the protective effects of antibodies".
The only thing that is unclear at this point is what it is you find so confusing.
____________________
Notes:
Callaway, Ewen. "Had COVID? You’ll probably make antibodies for a lifetime". Nature. 26 May 2021. Nature.com. 5 March 2022. https://go.nature.com/3HMZbmW
MacDaragh Ryan, Paul, and Noel M. Caplice. "Is Adipose Tissue a Reservoir for Viral Spread, Immune Activation, and Cytokine Amplification in Coronavirus Disease 2019?". Obesity. 31 May 2020. NCBI.NLM.NIH.gov. 5 March 2022. https://bit.ly/3HJesFt
Neurath, Markus F., Klaus Überla, and Siew C. Ng. "Gut as viral reservoir: lessons from gut viromes, HIV and COVID-19". Gut. 26 April 2021. Gut.BMJ.com. 5 March 2022. https://bit.ly/3hEHlIk
