You are trying to develop a more effective immunization against rabies. To be double sure that the immune system recognizes your immunization as foreign, you add plastic$-$aluminum micro$-$pellets to your immunization mixture. You also add pulverized, purified samples of rabies pathogens in your immunization mixture. You begin trials and discover that your vaccine completely prevents rabies symptoms in any animal treated with your vaccine prior to rabies exposure, and that no animals catch rabies from your vaccine. All animals treated with this vaccine become highly allergic, with lethal consequences, to any plastic$-$aluminum exposure, though. What went wrong?

All of these explanations describe mechanisms that could have resulted in the allergy $($excess of course for the "none of these" answer$)$

Actually, this story makes it clear that the rabies pathogen uses plastic$-$aluminum for its antigens instead of structures such as glycoproteins, lipoproteins, etc. The plastic$-$aluminum is triggering a myeloid progenitor response which subsequently leads to dendritic cell multiplication and follows with macrophage over$-$produced antibody levels.

None of these explanations describe mechanisms that could have resulted in the allergy.

In addition to generating memory B cells, memory T cells, and memory plasma macrophages against rabies antigens, the animals also produced abundant levels of memory B cells, memory T cells, and memory plasma macrophages against plastic$-$aluminum. Now any exposure to plastic$-$aluminum elicits a massive immune response in the immunization treated animals, as if the plastic$-$aluminum was a dangerous pathogen.

In addition to generating memory B cells against rabies antigens, the animals also produced abundant levels of memory $B$ cells against plastic$-$aluminum. Now any exposure to plasticaluminum elicits a massive immune response in the immunization treated animals, as if the plastic$-$aluminum was a dangerous pathogen.