Type II hypersensitivity (antibody against cells) !

Process

Antibodies stick to the body's own cells or tissue. They mark them for destruction, or they switch a receptor on or off without killing the cell.

Updated 2026-11-01

See it in 3D: Thyroid gland · Spleen

What it is

In type II hypersensitivity, IgG or IgM binds an antigen that is fixed on a cell surface or in the extracellular matrix. The bound antibody can trigger complement, flag the cell for phagocytes in the spleen and liver, recruit NK cells (ADCC), or act on a receptor directly. It explains blood-group reactions, many autoimmune cytopenias and two classic receptor diseases, Graves disease and myasthenia gravis.

Key facts

Antigen is fixed on a cell or matrix; in type III it is soluble and travels in complexes.
Pernicious anemia is also type II: antibodies against intrinsic factor and gastric parietal cells.
Drugs can bind red cells or platelets and turn them into targets (drug-induced hemolytic anemia or thrombocytopenia).

Type II mechanisms with examples

Mechanism	What happens	Disease	Target antigen
Complement lysis and opsonization	Membrane attack complex bursts the cell, or C3b and IgG mark it for macrophages	Acute hemolytic transfusion reaction, autoimmune hemolytic anemia, hemolytic disease of the newborn	ABO and Rh antigens on red cells
Antibody-dependent cellular cytotoxicity (ADCC)	NK cells and macrophages bind the antibody's Fc and kill the coated cell	Immune thrombocytopenia	Platelet glycoproteins
Complement-driven inflammation	C5a recruits neutrophils that damage the tissue	Anti-GBM disease (Goodpasture), acute rheumatic fever	Type IV collagen; streptococcal M protein cross-reacting with cardiac myosin
Receptor stimulation	Antibody turns the receptor on without the hormone	Graves disease	TSH receptor
Receptor blockade	Antibody blocks and removes the receptor	Myasthenia gravis	Acetylcholine receptor at the neuromuscular junction
Loss of adhesion	Antibody separates cells from each other	Pemphigus vulgaris	Desmogleins

In the lab

Direct Coombs (direct antiglobulin) test: detects IgG or complement already on the patient's red cells.
Indirect Coombs test: detects free antibodies in serum, used in crossmatch and prenatal screening.

Test yourself

Think of the answer, then tap the question to see it.

What is the target of the stimulating antibody in Graves disease?

The TSH receptor on thyroid cells. The antibody mimics TSH, so the gland grows and makes too much hormone.

Which test shows that a patient's own red cells are coated with antibody or complement?

The direct Coombs (direct antiglobulin) test. It is positive in autoimmune hemolysis, hemolytic transfusion reactions and hemolytic disease of the newborn.

How does antibody-dependent cellular cytotoxicity kill a cell?

NK cells or macrophages grab the Fc tail of IgG bound to the cell and release perforin and granzymes, killing it without complement.

In myasthenia gravis, why is muscle weakness worse with repeated use?

Antibodies block and reduce acetylcholine receptors, so with repeated firing too few receptors respond and contraction fades.

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See it in 3D

The structures of Durgical's 3D anatomy where it is found.

Microorganisms

Streptococcus pyogenes

← All of immunology

Educational content on the immune system; not a treatment or individual vaccination guide and no substitute for a health professional's advice. No doses are given.

Sources: Type II Hypersensitivity Reaction (StatPearls Publishing (NCBI Bookshelf), 2025); Autoimmune responses are directed against self antigens (Garland Science (Janeway's Immunobiology, 5th ed., NCBI Bookshelf), 2001); ABO Blood Group System (StatPearls Publishing (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.