Your immune system doing too much. Four ways to overreact, and boards will test every single one.
Your immune system has four distinct modes of going too far. Boards want you to know which mechanism produces which disease. The secret: think about the timing and the mediator.
Types I-III use antibodies (humoral). Type IV uses T-cells (cell-mediated). That's your first fork. 🔑ABC = Antibodies for types 1-2-3. Type 4 = 4gotten antibodies (T-cells only).
Types I-III are antibody-mediated (humoral immunity). Type IV is T-cell mediated (cellular immunity). This is the single most important fork for classification.
Antibody: IgE
Timing: Minutes · this is the fast one
Mechanism: Antigen cross-links IgE on mast cellsTissue-resident immune cells loaded with granules of histamine, heparin, and proteases. They sit in connective tissue near blood vessels and at body surfaces · stationed at the borders, waiting for the signal to explode. → degranulation → histamine flood
Two phases:
Classic diseases:
Anaphylaxis can have a biphasic reaction. Patient gets epi, feels better, goes home · then crashes 4-8 hours later from the late phase. That's why you observe for hours after anaphylaxis. Boards love this.
Antibody: IgG or IgM
Timing: Hours to days
Mechanism: Antibodies bind to antigens on the cell surface → cell gets destroyed by complement or NK cells (ADCC). The target is the cell itself.
Three subtypes (boards love these):
Disease list:
Antibody: IgG (sometimes IgM)
Timing: Hours to weeks
Mechanism: Antibodies bind soluble antigens floating in blood → form immune complexes → complexes deposit in tissues (joints, kidneys, vessels) → complement activation → neutrophil recruitmentComplement fragments C3a and C5a are chemoattractants. Neutrophils arrive and release proteases and reactive oxygen species trying to destroy the complexes · but the tissue gets caught in the crossfire. That's the damage. → tissue damage
Key difference from Type II: Type II = antibody binds cell surface antigen (fixed). Type III = antibody binds soluble antigen (floating, clumps, deposits wherever blood flow slows).
Classic diseases:
Serum sickness = actual immune complexes (Type III). Caused by foreign proteins (antithymocyte globulin, infliximab).
Serum sickness-LIKE = clinically identical but caused by drugs (penicillin, cefaclor). No immune complex deposits on biopsy. Boards test this distinction.
Antibody: NONE · T-cells only
Timing: 48-72 hours (the slow burn)
Mechanism: Sensitized T-cells encounter antigen → release cytokines → macrophage activation → inflammation. No antibodies involved.
Two flavors:
Classic diseases:
TB skin test is read at 48-72 hours. Not 24. Not immediately. Measure the induration (not redness). If they ask when to read the PPD, the answer is always 48-72h because Type IV = delayed.
| Feature | Type I | Type II | Type III | Type IV |
|---|---|---|---|---|
| Mediator | IgE | IgG/IgM | IgG/IgM | T-cells |
| Timing | Minutes | Hours-days | Hours-weeks | 48-72 hrs |
| Target | Mast cells | Cell surface Ag | Soluble Ag | Tissue cells |
| Complement? | No | Yes | Yes | No |
| Key cells | Mast cells, basophils | NK cells, macrophages | Neutrophils | Macrophages, T-cells |
| IF pattern | N/A | Linear | Granular | N/A |
| Buzzword | "Anaphylaxis" | "Autoantibody" | "Immune complex" | "Granuloma" |
| Board classic | Bee sting → epi | Graves'/MG | SLE nephritis | PPD at 48-72h |
Each type has a signature disease. Tap a card to see the mechanism, mediator, and classic board presentation.
Anaphylaxis / Allergic rhinitis
Anaphylaxis, hay fever, asthma, urticaria
Treat: Epinephrine for anaphylaxis
No complement activation
Goodpasture / Graves / MG
Goodpasture, Graves, MG, AIHA, ITP
Functional: stimulatory (TSI) or blocking (AChR)
SLE / Serum sickness / PSGN
SLE, serum sickness, PSGN, Arthus rxn
Serum sickness: 7-14 days post-exposure
PPD / Contact dermatitis / Granuloma
TB PPD, contact dermatitis, GVHD, MS, T1DM
PPD read at 48-72h. No complement.
Four types. One axis: timing. The faster the reaction, the more preformed the mediator. Type I fires in minutes because the IgE + mast cell complex is already loaded. Type IV takes days because T-cells must first proliferate and then migrate to the site.
Read this diagram left to right: minutes → hours → days. Each row = one type. The colored bar = the reaction window. The icon = the key mediator. The label = what's being activated.
Timing tells you the type. Minutes = Type I. Hours = Type II or III. Days (48-72h) = Type IV. When the boards say "48-72 hours later," they are screaming Type IV at you.
Serum sickness (Type III) appears 1-3 weeks after the first exposure to a foreign protein because that's how long it takes to make enough IgG + antigen complexes. On re-exposure (already sensitized), it's faster: 2-4 days. Boards will test the "first exposure vs. re-exposure" distinction.
Both use IgG. Both activate complement. Boards will test whether you know the difference.
Type II: Antibody binds antigen stuck to a cell surface. The cell is the target. → Linear IF
Type III: Antibody binds antigen floating free in blood. They clump and deposit in tissues. → Granular IF
Type II is a targeted assassination (antibody finds the cell and kills it). Type III is collateral damage (immune complexes rain down wherever they land).
Linear IF = Type II (antibody coating the membrane uniformly). Granular IF = Type III (complexes depositing randomly). This single finding can answer the question.
Tap a disease, then tap the type it belongs to. 16 diseases. Go.
Patient has a suspected hypersensitivity reaction. Walk through it.
5 scenarios. Each clue eliminates one type. Last one standing wins. Or just guess early if you're feeling brave.
Start with timing. Work down. One click per branch.
4 patients with immune systems that can't chill. Don't make it worse. Different questions every reload.
Original board-style vignettes. Shuffled, never-repeat, full explanations for every choice.