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miljenko

07/17/20 3:04 PM

#233690 RE: Doc328 #233689

Thanks Doc.

I may need some time (learning, actually I am too old to start learning molecular biology, but I may try...) to digest what you wrote.

My idea was to understand why Oxford vaccines (whole spike, with adjuvant, viral vector) would generate stronger cellular response than mRNA based vaccines? Also, which may be better, modified S1 (MRNA) or S-RBD (PFE)? I do not easily buy simple PR from each company, as well *selective* publication material that may mislead true story.

Anyway, wish that all vaccine candidate works, and that World may come out (quickly) of today misery.
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linhdtu

07/18/20 12:50 PM

#233705 RE: Doc328 #233689

Thank you Doc for your kindness to take time to explain to common people like us.

Pretty darn good explanation btw. I get it or I think I get it, hence I get it :)
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vinmantoo

07/19/20 12:50 PM

#233726 RE: Doc328 #233689

The CD40/CD40L interactions from these now activated CD4 T cells (with cytokine help also), in turn cause Ig class switching so that these interactions reinforce each other.



Doc328, thanks for that very nice summary. Let me add that once the B cell has rearranged and class switches, there is a selection where cells whose BRC binds the antigen the tightest are stimulated to divide more. That means those with the strongest binding start predominating in the population. In addition, cells employ a targeted mutagenesis of the DNA segments which encode the variable regions of the antibody. Theses small changes can produce progenitor cells with stronger, the same or weaker antigen binding, and again the stronger binders will proliferate more. Thus, the antibody response gets stronger and more potent with time. Of course this antibody response needs to be eventually dampened down or resources will be wasted or possibly autoimmune responses can arise, but that is another story.