A Type II hypersensitivity reaction is an antibody-mediated immune reaction in which IgG or IgM antibodies bind to antigens on the surface of a person’s own cells or tissues, leading to cell destruction, inflammation, or dysfunction.
It is also called a cytotoxic hypersensitivity (although not all Type II reactions kill cells; some alter function).
IgG
IgM
Cell-surface antigens
(e.g., RBCs, WBCs, platelets, basement membranes, receptor proteins)
Type II reactions cause damage through one or more pathways:
Antibodies bound to cells activate complement → cell destruction.
Example: Autoimmune hemolytic anemia
IgG-coated cells are cleared by macrophages in spleen/liver.
Example: Hemolytic disease of the newborn (Rh incompatibility)
NK cells kill antibody-coated targets.
Antibodies block receptors (e.g., myasthenia gravis blocks ACh receptors)
Antibodies stimulate receptors (e.g., Graves disease stimulates TSH receptor)
Maternal IgG anti-Rh antibodies destroy fetal RBCs.
Anti-RBC antibodies → hemolysis.
Anti–basement membrane antibodies attack kidneys + lungs.
Antibodies block acetylcholine receptors → muscle weakness.
Antibodies stimulate TSH receptor → hyperthyroidism.
Antibodies react to mismatched donor RBCs → hemolysis.
Type II hypersensitivity = IgG or IgM antibodies directed against cell-surface antigens → cell destruction or dysfunction
If you want, I can compare all four types of hypersensitivity in a table.
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Type 2 hypersensitivity reactions occur when the immune system mistakenly identifies its own host cells or tissues as foreign and attacks them.
This reaction is mediated by antibodies, usually IgG or IgM, that bind to antigens on the surface of target cells or tissues, leading to destruction or dysfunction of those cells.
The binding of these antibodies activates the complement system and other immune mechanisms, leading to the destruction of the targeted cells.
The antigens that trigger type 2 hypersensitivity reactions can be intrinsic or extrinsic.
Intrinsic antigens are self-antigens that are expressed on the surface of normal cells, but the immune system recognizes them as foreign because they are structurally altered, as in autoimmune disorders.
Extrinsic antigens are foreign antigens that are present on the surface of host cells, as in the case of drug-induced immune reactions.
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Examples of type 2 hypersensitivity reactions include autoimmune hemolytic anemia, in which antibodies bind to and destroy red blood cells, and Goodpasture's syndrome, in which antibodies attack the basement membrane of the kidney and lungs. Other examples include transfusion reactions, where the immune system attacks donor blood cells, and drug-induced reactions, where the immune system attacks host cells that have been modified by drugs.
[Type 2 hypersensitivity reactions can cause a range of symptoms, depending on the type and severity of the reaction. These can include anemia, hemolysis, organ damage, and in severe cases, anaphylaxis or shock. Treatment may involve avoiding the triggering antigen, suppressing the immune response with drugs, or replacing damaged or destroyed cells or tissues.]
These are antibody-mediated hypersensitivity reactions and involve the activation of complement system by IgG or IgM antibodies directed against specific cell surface or extracellular matrix antigens. The complement activation then leads to destruction of the targeted cells. Examples of type II hypersensitivity reactions include autoimmune hemolytic anemia or Goodpasture's syndrome.
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Mechanism: IgG or IgM antibodies bind to antigens on cell surfaces → leads to complement activation or antibody-dependent cytotoxicity.
Examples:
Autoimmune hemolytic anemia
Goodpasture’s syndrome
Hemolytic disease of the newborn
Injury: Cell lysis or phagocytosis of targeted cells.
1. **Antigen Recognition**: Antigens, which are typically present on the surface of cells or extracellular matrix, are recognized by antibodies.
2. **Antibody Binding**: IgG or IgM antibodies bind to these antigens, forming an antigen-antibody complex.
3. **Complement Activation**: The binding of antibodies activates the complement system, a group of proteins that assist in destroying the target cell.
4. **Cell Lysis or Opsonization**:
- **Cell Lysis**: The complement system forms a membrane attack complex (MAC) that creates pores in the cell membrane, leading to cell lysis.
- **Opsonization**: Complement proteins and antibodies mark the cell for phagocytosis by immune cells such as macrophages and neutrophils.
### Examples of Type II Hypersensitivity Reactions
1. **Hemolytic Anemia**: The immune system targets and destroys red blood cells, leading to anemia.
2. **Goodpasture's Syndrome**: Antibodies target the basement membrane in the kidneys and lungs, causing damage to these organs.
3. **Graves' Disease**: Antibodies target the thyroid-stimulating hormone (TSH) receptor, causing hyperthyroidism.
4. **Rheumatic Fever**: Antibodies formed against streptococcal bacteria cross-react with heart tissue, causing inflammation and damage.
### Clinical Manifestations
- **Hemolysis**: Destruction of red blood cells leading to symptoms like fatigue, pallor, and jaundice.
- **Inflammation and Tissue Damage**: Resulting from the immune attack on target tissues, leading to organ-specific symptoms based on the affected tissue (e.g., kidney dysfunction in Goodpasture's syndrome).
Treatment typically involves immunosuppressive therapies to reduce the immune response and managing the symptoms of the specific condition.
Summary Table
Type Type 1 Type 2 Type 3 Type 4 Reactant IgE IgG IgG T effector cells Mechanism Mast-cell activation releases histamines and other mediators Antigens embedded in host cells cause complement activation and destruction by MAC. Antibody binds to soluble antigen, forming a circulating immune complex lodges in a vessel wall and causes a local inflammatory response. APC activates Th1/CTL. T cells activation macrophages and cause an inflammatory response. Time course Minutes Days Example Anaphylaxis Acute Transfusion Reaction Rheumatoid Arthritis, Vasculitis, Glomerulonephritis Contact Dermatitis, Mantoux tuberculin test
Mechanism: IgG or IgM antibodies bind to antigens on cell surfaces → leads to complement activation or antibody-dependent cytotoxicity.
Examples:
Autoimmune hemolytic anemia
Goodpasture’s syndrome
Hemolytic disease of the newborn
Injury: Cell lysis or phagocytosis of targeted cells.