The basics as far as I can tell: I inhale, say, juniper pollen. Something in the membrane of my nose/mouth/throat/lungs perceives the pollen as an immediate threat. Coughing, sneezing, eye irritation, great unpleasantness ensue. It’s like what would happen if my body detected a threatening virus or bacteria, only more. My questions:
What is it that detects something not in my blood and deems it a threat? I feel like I should remember this from high school bio, but I don’t.
What part of the body regulates how much of a reaction you have? I walk outside on a cold, dry day and my nose starts to run as a precaution. I walk outside on a spring day with a high pollen count, and my body goes into ‘all hands on deck’ mode, and I’m in danger of drowning on my own bodily fluids. Is it something going wrong in my brain? Is it purely a cellular-level response? Some things only warrant a relatively mild reaction (the wrong laundry detergent makes me a bit itchy), others can make me so miserable I don’t want to get out of bed (have I mentioned that juniper is a horrible, evil thing that I hate?). What decides how dangerous a given substance is?
This is going to be a cursory explanation; I’m sure someone will come along and do a better job.
Basically, you have antibodies in your body that are tuned to various things. Some of them are tuned to particular infectious agents that you’ve previously encountered, and some of them aren’t particularly tuned to anything. They’re just randomly generated and tested out for a while to make sure that they don’t react to your own cells. So, theres a bunch of random not-NinjaChick antibodies out there, and if one of them doesn’t much like the surface protein of a pollen particle, it’ll attach and your immune system will spring into action to defeat the evil invading pollen.
That said, I’ll try to break it down at least a little bit, till someone smarter comes along with better info.
Basically, it’s an overreaction from your immune system. When faced with an invader, your body has certain defense mechanisms. Inflammation, where cells infiltrate an area to attack. Production of mucus or tears, to flush things out of your mucus membranes. That sort of thing.
Specifically, it’s immune cells that are doing the patrolling and checking whether things are foreign. In your skin and mucus membranes, you have cells whose job is basically to pull apart viruses, bacteria, pollen, etc., and present them to white blood cells, who will decide whether or not they’re something to be dealt with. you also have something called “mast cells” which are basically little bags of histamine and in some people, with some antigens, are on a hair trigger. Those babies pop, and you have vasodilation, bringing fluid to the site, so your eyes get puffy and your nose feels blocked, and they can cause bronchoconstriction, so it’s a bit harder to breathe sometimes.
It’s not a brain thing, it’s your body’s first line of defense trying to do its job, and going a little overboard. But it’s just trying to help!
As for why some substances cause an allergic reaction, and some don’t, and it affects all people differently, it’s a long story and I forget a good bit of it, my immunology class having been about 6 years ago by now.
I’m taking the class now, so let me take a stab at it.
Allergy is more technically called Type-1 (Immediate) Hypersensitivity. The basic cascade of events is thus:
#1: Your body’s B-cells produce antibodies randomly. (Mostly randomly. There’s various selection procedures in place to keep self-reactive antibodies from being produced.) Each mature naive B-cell produces one specific antibody.
#2: Your body’s T-cells have randomly constructed T-Cell Receptors (TCRs). (Again, mostly randomly. There are selection procedures in place.)
#3: You encounter some molecule someplace. Maybe you get stung by a bee. Maybe you ate a peanut. Whatever. That molecule gets picked up by a professional antigen-presenting cell (APC - usually a dendritic cell) and shipped to a lymph node. The APC flags this molecule - the antigen - as some ‘type’ by expressing costimulatory molecules.
#4: By random chance, there’s a T-cell receptor out there that is just the right shape to lock onto the piece of antigen that the APC is presenting on its MHCII molecule (Major Histocompatibility Complex II. Don’t worry about it.). The APC is also expressing costimulators that flag this antigen as coming from some specific type of baddie, and that means that the T-Cell has just got two signals:
–DANGER! THIS MOLECULE IS EVIL!
–THIS MOLECULE CAME FROM ENEMY TYPE X!
That type, in case of allergens, is “worm”, or more generally any multicellular parasite. The T-cell now converts into action mode of a specific type: it differentiates into a T-Helper Cell type 2 (Th2), and is now ready to marshal a response.
#5: Some of the antigen gets to a B-cell that, again by random chance, produces an antibody that will bind to it. These antibodies are anchored to its surface and once something binds to them, they’ll get internalized, and the antigen processed and presented on the MHCII (there it is again - yes, it means that a B-cell is technically an APC, though of a pretty weak type).
#6: Things are coming into place. The activated Th2 cell is now reproducing, making copies of itself. All of them will be specific to a particular chunk of antigen being presented on an MHCII molecule. One clone gets in contact with the B-cell that we saw in Step 5, and locks onto it. The B-cell is now told: what you just picked up is EEEEEEVIL! It came from a worm! You know how to kill it! KILL KILL KILL!
#7: The B-cell now knows that it’s got something. It knows that it came from a specific enemy, and that enemy gets a specific kind of antibody: IgE. It goes through “isotype switching”, where it converts itself to the dedicated production of IgE that is specific to the antigen that it encountered. It also goes through “affinity maturation”, a process of directed evolution that makes the antibodies even more potent. It clones itself many, many times, and all of its progeny pump out that specific molecule of IgE.
#8: This IgE floats around, and encounters mast cells. Remember those from previous posts? The IgE binds to the mast cells, coating them. These guys live in places where they’re likely to encounter more antigen, and because they’re now coated with SPECIFIC IgE, they will react to THAT PARTICULAR ANTIGEN.
That antigen, by the way, is now an ALLERGEN.
#9: You get stung by a bee again, or eat another peanut, or whatever. It sucks to be you: your body’s defenses are now primed. They’ve made their enemy’s measure. They’re not going to let those damned peanuts through! The moment that allergen molecule encounters a primed mast cell, the IgE antibodies on it bind to the allergen and cross-link. The mast cell detects this and triggers, releasing histamine and various others pro-inflammatory molecules. The cascade has begun. Depending on how bad it is, you might get the sniffles, or you might go into anaphylactic shock - or anything in between.
Now, the question is, why does your body react to a harmless peanut as if it were an invading parasite?
I’d like to further this line of inquiry. Why is it that things like pollen can have tolerances built up for them in some people, yet this cannot be with foods? Is it because of the nature of the reactions themselves, it isn’t wise to continue exposing a person with a food allergy to the allergen because it is too dangerous? I guess ingesting the food means the systemic reaction will be bigger? I wonder if they ever will find a therapy that will help with food allergies. Is there research being done on this?
There are treatments that will desensitize a patient to a particular allergen. The current one is, I think, LDA (Low Dose Allergen Immunotherapy), which basically involve giving a person low doses of a given allergen over long periods of time. The levels are titrated sufficiently low so as not to trigger any huge reaction (so you’ll trigger just a few mast cells). The idea is that you’ll switch the presentation of that antigen from the “worm” costimulator to the “suppress” costimulator. The body will then develop a population of T-suppressor cells, which will actively work to prevent this hypersensitivity. T-suppressor cells are rather poorly understood, and I personally know very little about them, so I can’t say much.
No, you can’t just eat tiny amounts of peanuts and hope for the best. Hie thee to an allergist-immunologist.
Yep, alreadyon it. Getting the apointments set up for the shot therapy for the maple mix, short ragweed, and molds (etc.?) also. That was sort of wishful thinking, and sort of: Give me a little more than a layman’s “this is so” understanding of the mechanics that make the “why” so, is a way to put it. :o