Type II & Type III Hypersensitivity – Key Vocabulary

25 English vocabulary flashcards covering definitions and mechanisms related to Type II and Type III hypersensitivity reactions, their antibodies, effector pathways, and clinical examples.

Type II hypersensitivity

Antibody-mediated reaction in which IgG or IgM bind directly to antigens on host cell surfaces or basement membranes, leading to cell-specific damage.

Type III hypersensitivity

Immune-complex-mediated reaction in which circulating antigen–antibody complexes deposit in tissues, activate complement, and trigger inflammation.

IgG

The main immunoglobulin class involved in both type II (cell targeting) and type III (immune complexes) hypersensitivity reactions.

IgM

Pentameric antibody that can initiate complement activation; participates in type II hypersensitivity against cell surface antigens.

Complement system

Cascade of serum proteins (e.g., C3, C5–C9) that, once activated by antibodies, causes cell lysis, opsonization, chemotaxis, and inflammation.

Membrane Attack Complex (MAC)

Complement components C5b-C9 that insert into cell membranes causing osmotic lysis during type II reactions.

Opsonization

Tagging of particles or cells (e.g., RBCs) with antibody and/or C3b to enhance phagocytosis by neutrophils or macrophages.

Antibody-dependent cellular cytotoxicity (ADCC)

Killing of antibody-coated target cells by NK cells releasing perforin and granzymes.

Effector cells

Immune cells (neutrophils, macrophages, eosinophils, NK cells, platelets) that execute tissue damage after antibody or complement tagging.

Autoimmune haemolytic anaemia

Type II disease in which auto-antibodies bind to self-RBCs, activate complement, and cause haemolysis and anaemia.

Direct antiglobulin (Coombs) test

Diagnostic test that detects antibodies or complement bound to patient RBCs by observing agglutination after adding anti-human Ig.

Rhesus haemolytic disease of the newborn

Type II maternal-fetal reaction where Rh-negative mother produces anti-Rh IgG that crosses placenta and lyses Rh-positive fetal RBCs.

ABO transfusion reaction

Acute haemolysis caused by naturally occurring IgM antibodies binding to incompatible donor blood group antigens (type II hypersensitivity).

Immune complex

Lattice of antigen bound to antibody; normally cleared but can precipitate in tissues during type III hypersensitivity.

Solubilisation

Complement-mediated coating of immune complexes to keep them small and attach them to CR1 on RBCs for clearance.

Kupffer cells

Specialised liver macrophages that remove immune complexes transported by RBCs to the liver.

Site of complex deposition

Tissues such as kidney glomeruli, joints, skin, lung, or vessel walls where immune complexes lodge and incite inflammation.

Persistent infection

Source of continuous microbial antigen leading to chronic immune-complex formation in type III hypersensitivity.

Autoimmunity (type III context)

Production of antibodies against self antigens that form circulating immune complexes causing systemic damage (e.g., SLE).

Serum sickness

Systemic type III reaction to foreign serum proteins, characterised by fever, rash, arthralgia, and complement consumption.

Arthus reaction

Localized cutaneous type III hypersensitivity where injected antigen forms immune complexes with pre-existing antibodies, causing vasculitis.

Phagocytosis frustration

Condition in type II reactions where neutrophils cannot engulf large antibody-tagged targets, releasing granule enzymes onto surrounding tissue.

Basement membrane antibody

Auto-antibodies that target collagen or other components of basement membrane, provoking complement activation and tissue damage (type II).

Complement receptor 1 (CR1)

Receptor on RBCs that binds C3b-coated immune complexes, transporting them to liver and spleen for clearance.

Hypersensitivity

An exaggerated or inappropriate immune response that results in tissue damage rather than protection.