Answers: 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 cell. They only generate IgM, and sometimes IgA, IgG2. The B1 generate the so call "natural antibodies".
Only B2 lymphocytes can be activate by Th2 cells and form a lower follicle in lymphoid tissue and for this reason by the mechanism of screening, the ones with the better "affinity" for the antigen receive a survival signal by a T cell (apparently it's not drastically clear the nature of this cell Th1-Th2?) and trademark the isotopic switch to IgE (or IgG, etc.), since their first antibody is IgM. Only a small population of the B2 go their separate instrument and generate the initial IgM antibodies (low affinity) in the hasty stages of immune response.
Now, you said Haptenization Excluded, and that's the interesting part. The phenomenon of haptenization within combined vaccines (for example with a medication polysaccharides and a bacterial toxin, protein) is based within the immunological physiology. The protein allows the collaboration of Th2 cells near the B2, otherwise, if the vaccine was simply a Polysaccharides, the response would not last within 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 hard to please signals that makes the B cell alteration to IgE instead of IgGs. Apparently it has to do next to the interaction of this uncertain T cell within the folicle. Also, we know certain allergies relate to HLA haplotypes.