Lyrics · 完整歌詞
The classical hypersensitivity framework organises immune-mediated injury by the effector involved,
the target recognised and the mechanism through which damage occurs.
The Gell and Coombs framework yields four answers.
Type I is immediate and IgE-mediated, acting through mast cells within minutes.
Type II is antibody directed at cell-surface antigens,
either destroying the cell through complement or antibody-dependent cytotoxicity,
or altering receptor function.
Graves disease and myasthenia gravis belong here,
not to Type I or III.
Type III is deposition of immune complexes,
recruiting complement and neutrophils over days, as in serum sickness and lupus.
Type IV alone is antibody-independent.
T cells and macrophages produce contact dermatitis,
the tuberculin response and graft rejection at 48 to 72 hours.
Type I hypersensitivity is a two-act play.
In the sensitisation phase,
dendritic cells present the allergen to naive CD4 cells in an IL-4-rich environment,
which drives differentiation towards Th2.
IL-4 instructs B cells to switch class to IgE.
That IgE occupies the high-affinity receptor FcεRI on mast cells and basophils
and waits.
On re-exposure the allergen cross-links adjacent IgE molecules and triggers degranulation.
Preformed histamine and tryptase are released at once,
while leukotrienes C4 and D4 and prostaglandins are synthesised within minutes.
Smooth muscle contracts, vessels dilate and leak, and mucus pours.
Four to eight hours later, IL-5 recruits eosinophils for the late-phase response.
The immediate and late phases are therefore one mechanism in two tempos,
not two types.
The classical hypersensitivity framework organises immune-mediated injury by the effector involved,
the target recognised and the mechanism through which damage occurs.
Anaphylaxis is that mechanism expressed systemically,
and its treatment has a single first line.
Adrenaline at 0.01 mg/kg,
to a maximum of 0.5 mg of the 1:1000 solution,
is injected intramuscularly into the anterolateral thigh
and repeated every five minutes if needed.
Alpha-1 stimulation restores vascular tone, beta-1 supports the heart, beta-2 relaxes bronchi,
and mast cell release is suppressed.
The patient lies flat, because standing can precipitate cardiovascular collapse.
Oxygen and 20 mL/kg of crystalloid follow for hypotension.
Antihistamines relieve only itch, corticosteroids have no proven role,
and intravenous bolus adrenaline is reserved for cardiac arrest.
Serum tryptase within one to two hours, compared with a baseline sample,
confirms mast cell degranulation.
Not every swelling is histamine.
Chronic spontaneous urticaria itches, wheals and responds to second-generation antihistamines,
escalated to four times the licensed dose and then omalizumab.
Hereditary angioedema, by contrast, is painless, non-itchy and unresponsive to antihistamines,
because deficient C1 inhibitor allows bradykinin to accumulate.
A low C4 level screens for it,
and treatment is C1 inhibitor concentrate or icatibant.
Allergic diseases are rising as environments become cleaner.
The hygiene hypothesis proposes that reduced microbial exposure in infancy leaves Th1 immunity underdeveloped
and tilts the balance towards Th2.
Prolonged antibiotic use therefore increases, rather than reduces, the risk of asthma.
House dust mite remains the most important inhaled allergen,
and it is visible under an ordinary light microscope.
The classical hypersensitivity framework organises immune-mediated injury by the effector involved,
the target recognised and the mechanism through which damage occurs.