Comprehensive Guide to Hypersensitivity Types and Immune Responses in Immunology

Normal immune response characteristics

Protective; regulated; eliminates pathogens with minimal host damage; promotes healing

Hypersensitivity response characteristics

Exaggerated or inappropriate immune response causing tissue damage

Why hypersensitivity occurs

Response to harmless or self antigens

Hypersensitivity classification

Type I, II, III, IV based on mechanism

Why two exposures needed for Type I hypersensitivity

First exposure causes IgE sensitization; second exposure triggers mast cell degranulation

Sensitization phase of Type I hypersensitivity

IgE production and binding to mast cells without symptoms

Effector phase of Type I hypersensitivity

Allergen cross-links IgE causing mast cell degranulation

Immunoglobulin involved in Type I hypersensitivity

IgE

Immunoglobulins involved in Type II hypersensitivity

IgG and IgM

Immunoglobulins involved in Type III hypersensitivity

IgG and IgM

Immune mediator of Type IV hypersensitivity

T cells (no antibodies)

IgE primary location

Bound to mast cells and basophils

IgG primary location

Serum and tissues; crosses placenta

IgM primary location

Intravascular

IgA primary location

Mucosal secretions

IgD primary location

B-cell surface

Preformed mediators in Type I hypersensitivity

Histamine, heparin, proteases, chemotactic factors

Histamine effects

Vasodilation, increased vascular permeability, bronchoconstriction

Inherited factors contributing to atopy

Increased IgE production; Th2 bias; family history

General treatment principles for Type I hypersensitivity

Avoidance; antihistamines; steroids; bronchodilators; epinephrine

Mechanism of Type II hypersensitivity

Antibody binding to cell surface antigens causing cell destruction or dysfunction

Effector mechanisms in Type II hypersensitivity

Complement activation, opsonization, ADCC

Examples of Type II hypersensitivity

Autoimmune hemolytic anemia; Goodpasture syndrome; myasthenia gravis; Graves disease

Examples of Type III hypersensitivity

SLE; post-streptococcal glomerulonephritis; serum sickness; Arthus reaction

Mechanism of Type III hypersensitivity

Immune complex deposition causing inflammation

Order of events in Type III hypersensitivity

Immune complex formation → deposition → complement activation → neutrophils → tissue damage

Mechanism of Type IV hypersensitivity

T-cell mediated delayed response with macrophage activation

Timing of Type IV hypersensitivity

Delayed (24-72 hours)

Why Type I reactions do not occur on first exposure

No IgE cross-linking occurs during sensitization

Primary effector cells in Type I hypersensitivity

Mast cells and basophils

Role of eosinophils in Type I hypersensitivity

Late-phase inflammation and tissue damage

Role of Th2 cells in Type I hypersensitivity

Promote IgE class switching

Diagnostic tests for Type I hypersensitivity

Skin prick test; serum IgE; allergen-specific IgE

Type I hypersensitivity summary

Immediate; IgE mediated; mast cells

Type II hypersensitivity summary

Antibody-mediated cytotoxicity

Type III hypersensitivity summary

Immune complex mediated

Type IV hypersensitivity summary

T-cell mediated; delayed

Hypersensitivity definition

Exaggerated immune response causing tissue damage

Normal immune response goal

Eliminate pathogen with minimal host damage

Type I hypersensitivity mechanism

IgE-mediated mast cell degranulation

Type I requires two exposures

Sensitization then IgE cross-linking

Type I reaction timing

Immediate (minutes)

Key cells in Type I hypersensitivity

Mast cells, basophils, eosinophils

Key antibody in Type I hypersensitivity

IgE

Major mediator of Type I hypersensitivity

Histamine

Classic Type I examples

Anaphylaxis, asthma, allergic rhinitis, urticaria

Type II hypersensitivity mechanism

IgG/IgM against cell surface antigens

Type II effector mechanisms

Complement, opsonization, ADCC

Classic Type II examples

Autoimmune hemolytic anemia, Goodpasture, myasthenia gravis, Graves disease

Type III hypersensitivity mechanism

Immune complex deposition

Type III common sites

Kidneys, joints, blood vessels

Classic Type III examples

SLE, post-strep glomerulonephritis, serum sickness

Type III key sequence

Immune complexes → complement → neutrophils → damage

Type IV hypersensitivity mechanism

T-cell mediated delayed response

Type IV reaction timing

Delayed (24-72 hours)

Classic Type IV examples

Contact dermatitis, TB skin test, graft rejection

Antibodies involved in Type IV

None

Most important exam distinction

Type I = IgE; Type IV = T cells

IgE location

Bound to mast cells and basophils

IgG key feature

Crosses placenta

IgM key feature

Intravascular; first antibody made

IgA key feature

Mucosal protection

Type I treatment cornerstone

Epinephrine for anaphylaxis

Diagnostic test for Type I

Skin prick test

Atopy definition

Genetic tendency to produce IgE

Type I not seen on first exposure

Requires IgE sensitization

Summary of all four sensitivities

I = IgE immediate; II = cytotoxic; III = immune complex; IV = delayed T-cell