Hypersensitivity and Immunology

An exaggerated immune response to a normally harmless antigen that causes tissue damage.

A classification of four hypersensitivity types based on immune injury mechanisms, introduced in 1963.

Type I: immediate, anaphylaxis;
Type II: cytotoxic, immune mediated hemolytic anemia;
Type III: immune complex-mediated, glomerulonephritis
ype IV: delayed, T-cell-mediated, allergic contact dermatitis

Types I, II, and III involve antibodies; Type IV is T-cell-mediated.

Initial antigen exposure primes the immune system without causing an allergic reaction.

A subsequent exposure or persistent antigen may trigger an immune reaction.

second exposure

Yes, if the antigen persists after initial sensitization.

abnormal immune response to typically harmless substances
- most allergies are type 1

An antigen that causes an allergic reaction.

A genetic predisposition to develop IgE-mediated allergies against normally harmless substances (dust, pollen)

Ingestion, inhalation, percutaneous exposure, and skin contact.

IgE antibodies and mast cells.

Dendritic cells present allergens to naïve T cells, promoting Th2 differentiation and IgE production.

IL-4.

IL-5.

IgE binds mast cells, sensitizing them without causing degranulation.

Allergen cross-linking of mast cell-bound IgE during subsequent exposure.

They release major basic protein and eosinophil cationic protein, causing tissue injury.

IgG or IgM antibodies and complement.

Antibodies bind cell-surface antigens, causing cell destruction; cytotoxic effect

Neonatal isoerythrolysis, immune-mediated hemolytic anemia, and incompatible blood transfusion reactions.

An Aa-positive foal ingests anti-Aa antibodies from its sensitized Aa-negative mare's colostrum.

Maternal antibodies bind foal RBCs and activate complement-mediated hemolysis.

IgG or IgM antibodies target RBC surface antigens, causing RBC destruction.

Extravascular hemolysis by macrophages and intravascular hemolysis by complement.

A small molecule that becomes immunogenic when bound to a carrier; drugs can bind RBCs and trigger antibody-mediated destruction.

A hapten is a molecule too small to trigger the immune system on its own, but it becomes a target once it sticks to a bigger protein.


A drug is a sticker that glues onto the RBC surface and changes how it looks. The guard sees a "new" cell and attacks. The drug is acting as a hapten (small Lego piece clipped onto a big base).

Antigen-antibody immune complexes deposit in tissues, activate complement, and cause inflammation.

A systemic Type III reaction that developed approximately 10 days after administration.

Antibody excess promotes clearance; antigen excess favors complex deposition and tissue injury.

• Antibody excess: complement activates, and complexes are cleared by mononuclear phagocytes (the body handles it).
• Antigen excess: complexes are NOT cleared, so they deposit in blood vessel walls, activate leukocytes, and cause tissue injury.

Immune complex deposition, classical complement activation, and neutrophil recruitment causing tissue damage.

Immune complexes deposit in glomeruli, causing inflammation, structural damage, and impaired kidney function.

A Type III hypersensitivity reaction occurring 2–4 weeks after infection or vaccination, often involving Streptococcus equi, causing edema, urticaria, and hemorrhages.

T cells and myeloid cells, especially macrophages.

Delayed, generally 24–72 hours after exposure.

Detecting immune sensitization to mycobacterial antigens as part of tuberculosis control.

Haptens bind skin proteins, Langerhans cells present antigens to T cells, and activated T cells cause inflammation and keratinocyte damage.

Urushiol binds skin proteins to form neoantigens, triggering a delayed Type IV reaction after sensitization.

IL-31 from activated Th2 cells stimulates sensory neurons and keratinocytes, causing itching and inflammation.

Nickel acts as a hapten, binds skin proteins, activates T cells and macrophages, and causes keratinocyte destruction.

Hypersensitivity describes the immune injury mechanism; autoimmunity describes an immune response against self-antigens.

IMHA targets self-RBCs through Type II cytotoxicity; lupus nephritis involves self-directed immune complexes causing Type III injury.