Feb
Allergies as a hypersensitivity type I (IgE mediated)phenomenon, no. In my immunology book (published recently) says that the immune response to Polysaccharides is solely by B1 and B from the marginal spleen zone (BMZ) lymphocytes. Their activation do not require collaboration by Th2 cells. They only generate IgM, and sometimes IgA, IgG2. The B1 generate the so called "natural antibodies".
Only B2 lymphocytes can be activated by Th2 cells and form a secondary follicle in lymphoid tissue and therefore by the mechanism of selection, the ones with the better "affinity" for the antigen receive a survival signal by a T cell (apparently it's not very clear the nature of this cell Th1-Th2?) and make the isotopic switch to IgE (or IgG, etc.), since their first antibody is IgM. Only a small population of the B2 go their separate way and generate the initial IgM antibodies (low affinity) in the early stages of immune response.
Now, you said Haptenization Excluded, and that's the interesting part. The phenomenon of haptenization in combined vaccines (for example with a capsule polysaccharides and a bacterial toxin, protein) is based in the immunological physiology. The protein allows the collaboration of Th2 cells with the B2, otherwise, if the vaccine was only a Polysaccharides, the response would not last in time and it would be the low-affinity IgM (when the desired one is long-lasting IgG)
Also, adding a small detail, we still don't know clearly what are the particular signals that makes the B cell change to IgE instead of IgGs. Apparently it has to do with the interaction of this uncertain T cell in the folicle. Also, we know certain allergies relate to HLA haplotypes.