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Hypersensitivity reactions represent the immune system's "friendly fire"โwhen protective mechanisms cause harm instead of healing. You're being tested on your ability to distinguish which immune components drive each reaction type, how timing reveals mechanism, and why certain diseases cluster under specific hypersensitivity categories. These four types aren't arbitrary classifications; they reflect fundamentally different pathways involving distinct antibody classes, cell types, and effector mechanisms.
Don't just memorize that Type I involves IgE or that Type IV is T cell-mediated. Know why IgE-mast cell interactions produce immediate symptoms while T cell responses take 24-48 hours. Understand how the location of antigen (cell-bound vs. soluble vs. intracellular) determines which hypersensitivity pathway dominates. When an exam question describes a clinical scenario, you should be able to work backward from timing, symptoms, and mechanism to identify the reaction typeโthat's the conceptual skill being assessed.
These reactions depend on preformed antibodies and occur rapidly because the immune system has already been primed. The speed of response correlates directly with whether effector molecules are ready and waiting.
When antibodies target antigens fixed to cell surfaces, the immune system destroys those cells as if they were pathogens. The key distinction from Type I is that the antigen is cell-bound, not soluble.
Compare: Type I vs. Type IIโboth use antibodies as primary mediators, but Type I involves IgE triggering mast cells (soluble allergens), while Type II uses IgG/IgM to destroy cells bearing surface antigens. If an FRQ describes hemolysis or cytopenia, think Type II.
When antigen-antibody complexes form in circulation and deposit in tissues, they trigger inflammation at sites far from the original antigen encounter. Deposition location determines which organs suffer damage.
Compare: Type II vs. Type IIIโboth involve IgG antibodies, but Type II targets cell-surface antigens (destruction at the cell), while Type III involves soluble antigens forming complexes that deposit elsewhere (destruction at deposition sites). The antigen's location is your key differentiator.
Type IV stands apart because it involves no antibodiesโT cells are the sole mediators. The 24-48 hour delay reflects the time required for T cell activation, proliferation, and migration to the antigen site.
Compare: Type I vs. Type IVโboth can cause skin reactions, but Type I produces immediate wheals (minutes, IgE-mediated), while Type IV causes indurated erythema (days, T cell-mediated). Timing alone can distinguish them on an exam.
| Concept | Best Examples |
|---|---|
| IgE-mediated, immediate | Anaphylaxis, allergic asthma, hay fever |
| IgG/IgM targeting cell surfaces | Transfusion reactions, autoimmune hemolytic anemia, Goodpasture syndrome |
| Immune complex deposition | SLE, serum sickness, Arthus reaction |
| T cell-mediated, delayed | Contact dermatitis, tuberculin test, granulomatous diseases |
| Complement involvement | Type II (cell lysis), Type III (inflammation at deposition sites) |
| Mast cell involvement | Type I only |
| Requires prior sensitization | All four types, but clinically emphasized in Type I and Type IV |
A patient develops widespread urticaria and bronchospasm within 5 minutes of a penicillin injection. Which hypersensitivity type is this, and what antibody class is responsible?
Compare and contrast Type II and Type III hypersensitivity: both involve IgG, so what determines whether a reaction is classified as one versus the other?
A tuberculin skin test is read at 48 hours. Why would reading it at 4 hours give a false-negative result, and which immune cells are responsible for the positive reaction?
Which two hypersensitivity types would you consider if a patient presents with hemolytic anemia? How would you distinguish between them diagnostically?
An FRQ asks you to explain why anaphylaxis occurs within minutes while contact dermatitis takes days to develop. What mechanistic differences account for this timing distinction?