So does this mean that the immunologic memory is only limited to protein antigens?
as modeselektor mentioned a good way to understand this is to remember the two ways taht B cells get activated and how that relates to the difference between vaccines.
There are two ways for naive B cells to be activated after an antigen matches the IgM/IgD on their cell surface. Lets call the naive B cell who has that matching IgM/D "Bob."
1)
T cell Dependent: Lets say the antigen is a protein and thus has been processed by other APCs, such as a macrophage, and presented to T Cells via MHCII. Now there is a clonal population of these T cells with CD40L on their surface looking for B cells to activate. So there now many activated T cells running around and eventually one will find Bob. Remember B cells are APCs too, so Bob will show this protein antigen to the Activated T Cell, the second signal with CD40R (Bob) and CD40L (Tcell) will be activated, and Bob can now proliferate, undergo SHM, class switch, and form plasma cells and memory B cells.
2)
T cell Independent: Lets say the antigen is a polysaccahride or non peptide. Remember that MHCII (invariant chain and all that jazz) can only process peptide antigens. So there is no APC presenting this antigen on MHCII to T cells. But Bobs surface IgM/IgD has no such restriction, and if the antigen load is high enough and enough of his receptors cross link, he can activate himself without any T cell help. I believe he can then go on to produce IgG, but he does not get the affinity maturation or the other types of class switching, whihc are T cell dependent.
So you can have immunological memory to purely polysaccharide antigens, but it is purely humoral. This is why Kids<5 get the Conjugated pneumococcal vaccine, even though it covers less serovars, because their immune system is not mature enough to mount a full T cell independent response. Similarly, this is why inactivated/killed vaccines tend to require booster shots. A live attenuated vaccine, because it actually infects cells and there is presentation on MHCI and MHCII, produces a much more robust cell mediated response and the Th cells support a more robust humoral response. A killed vaccine, though ti has no chance of converting to a virulent strain, only produces a humoral response that has no T cell support. Hence booster shots.
Not all of this is completely logical...Things get complicated due to things like Cross presentation, but you can read up on it in that book, which is a great one.
Just to throw in some important B cell points:
1) Immature B cells undergo negative selection and VDJ/VJ recombination in the
Bone Marrow. This allows for their surface IgM to recognize a wide variety of antigens but not self.
2)
Somatic Hypermutation is the mechanism for affinity maturation. This occurs in the
LN Germinal Center during the Primary immune response and requires T cells. The B cell has already been activated, so the IgM can recognize the antigen, but SHM tweaks the DNA, witht eh result of either improving or worsening antigen recognition. Those changes which improve antigen recognition are positively selected for.
3)
Class Switching also occurs in the
LN germinal center during the late primary immune response and requires T Cells.
2 consequences to take note of:
1) On second exposure to an antigen, there is no need for class switching, as it has already taken place and you have memory B cells waiting to produce either IgG or IgA. So no IgM is made. Class switching is dependent on CD40L (Tcell) and CD40 (B cell) interaction. Therefore CD40L deficiency is a cause of Hyper IgM syndrome, an XLR immunodeficiency syndrome that presents with pyogenic abscesses and opportunistic infections early in life.
2) If there's a picture of a LN germinal center and they are asking what process is taking place, its either class switching or somatic hypermutation, not VDJ or VJ recombination.
