Apoptosis

I was wondering why a disease that causes mononucleosis is associated with polyclonal activation? Isn’t mononucleosis just a rise in the number of monocytes in the blood? B cells are the ones responsible for polyclonal activation, so why are they involved in this scenario?

Hey guys, I just wanna clear something up. 1. MHC molecule (alpha and beta chains) are held together by non-covalent interactions. 2. Is the peptide held on the hypervariable region of the MHC molecule by non-covalent interactions as well? 3. when the TcR binds to the peptide on the MHC and to the MHC itself, are they also non-covalent interactions? Thanks guys, I appreciate your input.

B220 is a surface marker on B cells. B220 is rather another name for CD45R, the ligand which is present on helper T cells that binds to CD22 on APC to activate T helper cells by cleaving phosphates off certain signalling molecules of the CD3 apparatus. This being so, does it not mean that B cells binds to APC? This confused me, as I knew of B cell – T helper cells interaction, but not the former. B cell itself is an APC, so it further does not make sense. Help?

I'm just wondering why MHCI specifically would be involved in allograft rejections... such as a kidney. My understanding is that since MHCI is found on all nucleated cells, it would be quite prevalent throughout the human body system, therefore easily detecting any foreign molecule. Then how would MHCII be involved in transplant rejections as well?