having a hypersensitivity means that someoneâ€™simmune system has reacted to something in such a way that it ends up damaging them,as opposed to protecting them. there are four different types of hypersensitivities,and in the first type or type one, the reactions rely on immunoglobulin e, or ige antibody,which is a specific type of antibody - the other major ones being igg, iga, igm, andigd. so because ige is involved with type one hypersensitivityreactions they are also called ige-mediated hypersensitivities. this type of reaction is also sometimes calledimmediate hypersensitivities, because the reaction happens super fastâ€”on the orderof minutes.
so most allergic reactions are ige-mediated,and therefore most allergies are type i hypersensitivity reactions. â€œallergyâ€ comes from the greek allos whichroughly means â€œotherâ€ and ergon which means â€œreactivityâ€. essentially, allergies are reactions to moleculesfrom outside your own body that most people donâ€™t react toâ€”and these are specificmolecules from things you might breathe or take in like foods, animal dander, bee stings,mold, drugs or medications, and pollen. you can also mount an allergic reaction tothings you come in contact with on your skin like latex, lotions, and soaps.
these specific molecules are also called antigens,and when they cause an allergic reaction, theyâ€™re called allergens. an allergic reaction happens in two steps,a first exposure, or sensitization, and then a subsequent exposure, which is when it getsa lot more serious. people that react to these allergens usuallyhave a genetic predisposition to having over-reactions to unknown molecules or allergens. this means that these people have certaingenes that cause their t-helper cells to be more hypersensitive to certain antigens. since the production of these t-helper cellsis genetically linked, allergies to things
tend to run in families. so letâ€™s say this person breathes in someragweed pollen, that person happens to have t-helper cells that can bind to a specificmolecule on the pollen, making that molecule an allergen. first off, that antigen gets picked up byimmune cells hanging out in the membranes along the airways, which then grab the moleculeand migrate to the lymph nodes, which happens regardless of if the person is allergic ornot. these cells are antigen-presenting cells,since they carry the antigen to the lymph nodes and present it to the t-helper cellsliving there.
dendritic cells and macrophages are examplesof antigen-presenting cells. when the person is allergic, the antigen presentingcell will also express costimulatory molecules, which are needed to mount an effective immuneresponse. before the t-helper cell sees the antigenthough, itâ€™s called a naive t-helper, since, even though itâ€™s built to recognize theantigen, it hasnâ€™t actually seen it before. when the t-helper gets its hands on the antigenthough, and also binds the costimulatory molecule, itâ€™s now been primed, and the naive t-helperchanges into a different sort of t-helper cell. usually in type i hypersensitivity it differentiatesinto a type 2 t helper cell, or just th2 cell,
and this step happens in response to varioussmall proteins or interleukins that might be floating around at the time. some interleukins that sway the t-helper cellinto turning into a th2 cell are interleukin 4, interleukin 5, and interleukin 10, andthese are all cytokines - and theyâ€™re given numbers because itâ€™s easier to keep trackof them that way. at any rate, the excited th2 cells releasea bit of their own interleukin 4 and get the b cells to undergo antibody class-switching,and so the b cell switches from making igm antibodies to making ige antibodies whichare specific to ragweed pollen in our example. th2 cells also release some interleukin 5,which stimulates production and activation
of eosinophils, a granulocyte, which is atype of white blood cell that degranulates or essentially releases a whole bunch of toxicsubstances that can damage both invading cells and nearby host cells. these ragweed-specific ige antibodies havea high affinity for, or basically really like fc epsilon receptors on mast cells, anothertype of granulocyte, so they quickly attach themselves to the surface of mast cells. these antibodies are also called cytotropicantibodies, since they can bind to cell surfaces. at this point itâ€™s like the mast cellâ€™sbeen geared up for combat, and is ready for action, and therefore weâ€™re finished withthe sensitization phase.
now letâ€™s say that that same person breathesin the ragweed pollen again, maybe a few months later - a second exposure. well, the suped up mast cells, using theircoat of antibodies, binds to the antigen. actually, it takes two or more bound antigensto cross-link the ige antibodies, which signals the mast cell to degranulate and release abunch of pro-inflammatory molecules called mediators that ultimately causes the effectsseen in an allergic reaction. one of the major mediators released in anallergic reaction is histamine. histamine binds to h1 receptors and causesthe smooth muscles around the bronchi to contract, which means the airways get smaller, makingit more difficult to breathe.
it also causes blood vessel dilation and increasedpermeability of the blood vessel walls, meaning that, while blood vessel diameter increasesand blood flow to the affected area increases, fluid is allowed to more easily leak out theblood vessel walls and get into the interstitium, the spaces between cells, which causes edemaand swelling, and urticaria, or hives. in addition to histamine, mast cells releaseother pro-inflammatory mediators including some that activate eosinophils and proteaseswhich chop up large proteins into small peptides. the effects of these molecules are calledâ€œearly phase reactionsâ€, and they happen within minutes of the second exposure. there are also â€œlate phase reactionsâ€though, which happen 8-12 hours after that
second exposure, where even more immune cellslike th2 cells, eosinophils, and basophils, yet another type of granulocyte, are recruitedto the site where the allergen is located because of the cytokines and pro-inflammatorymolecules produced during that early phase. these include some of those same interleukinsagain, interleukin 4, interleukin 5, and interleukin 10, but also leukotrienes which are smallermolecules made out of fatty acids and facilitate communication between a local group of cells. two leukotrienes in particular, ltb4 and ltc4,can not only cause smooth muscle contraction and damage to the epithelium like histamine,but they can attract immune cells - like neutrophils, mast cells, and eosinophils to their locationeven after the allergen is long-gone.
a lot of people with allergic reactions experiencemild symptoms, like hives, eczema, allergic rhinitisâ€”which is inflammation of the nose,as well as asthma. certain people though, when exposed to a largeload of specific allergens, like bee stings, seafood, or peanuts, can have a really severeand potentially life threatening allergic reaction. the increased vascular permeability, alongwith the constriction of airways can be severe enough such that the body canâ€™t supply thevital organsâ€”like the brain, with enough oxygen-rich blood, a condition known as anaphylacticshock. treatment for type one hypersensitivity caninvolve a variety of medications.
antihistamines, act to block the effects ofhistamine, which reduces vascular permeability and bronchoconstriction. also thereâ€™re corticosteroids, which canbe used to reduce the inflammatory response, as well as epinephrine, which is sometimesgiven during severe reactions via intramuscular injections through an epipen or intravenousinjection. epinephrine can help constrict blood vesselsand prevent anaphylactic shock. if thereâ€™s ever a serious type one hypersensitivityreaction that requires something like steroids or epinephrine, itâ€™s super important toget medical attention because type 1 hypersensitivity reactions can be serious and can sometimesget slightly better before getting worse again.