[possibilistic]

This is not how Type I hypersensitivity works. Epitope recognition is powered by a biological RNG (somatic hypermutation) and evolves at runtime via the process of somatic / V(D)J chain recombination. Your body learns to be allergic, perhaps due to a bad ashy vent (you got sick that one spring), under-stimulation (play outside!), or just plain bad luck. Unfortunately for all of us, the immune system has no concept of the innocuous nature of harmless antigens. It will continue to pick up bad habits until the day we die. But thankfully it also keeps the trillions of cells, leaky programming, our own broken and errant self, and other uninvited guests that would just as soon eat us at bay (bacteria, viruses, cancer, fungi, nematodes, ...).

[chaosfactor]

Did you just say that allergies are never genetic?

[possibilistic]

No. I described at a high level just one of the mechanisms of adaptive immunity--one of the most incredible biological systems in my opinion. (Runtime metaheuristics search!) These are complex pathways that involve many genes.

If the system isn't working you probably won't live very long. And while there may be certain functional alleles that may increase odds of an initial false positive stimulation, by in large the entire class of failure known as "allergic reactions" is simply a result of how the system itself works. You don't really need to invoke genetic differences to see how it fails. This is why the hygiene hypothesis is so strong.

There are actually four major categories of hypersensitivity that involve different cell populations and signalling pathways (eg. why poison ivy allergy is different from pine allergy).

If you're interested, the Wikipedia articles aren't a bad read. I also recommend Janeway's Immunobiology as a great intro to the entire subject.

[nooneelse]

Are "autoimmune disorders" another label for a class of failures of this search and respond system?