Type 2 – Hypersensitivity

by Peter Delves, PhD

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    Type II hypersensitivity is antibody against cell surface antigens. Examples of Type II hypersensitivity include transfusion reactions, autoimmune hemolytic anemia, pernicious anemia, hemolytic disease of the fetus and newborn, autoimmune thrombocytopenic purpura, acute rheumatic fever, Goodpasture syndrome, Graves’ disease and myasthenia gravis. There are antibody-mediated effects due to these antibodies binding to cell surfaces. This can lead to complement activation, and the activation of other white blood cells, in other words leukocytes. This results in complement and Fc receptor-mediated inflammation and tissue injury. Alternatively, antibody-mediated effects may result in abnormal physiological responses without cell and tissue injury. Two examples are given here. On the left hand side, we can see in an individual with a particular type of autoimmune disease called thyroid autoimmune disease, more specifically Graves’ disease which is one type of thyroid autoimmune disease. That this individual has antibodies that are binding to the thyroid stimulating hormone receptor, the TSH receptor that is present on the surface of thyroid epithelial cells. These autoantibodies, because they are antibodies being produced against a self antigen, the TSH receptor. These antibodies stimulate the receptor without needing any TSH there at all. So there’s a constant stimulation of the thyroid gland and an overproduction of thyroid hormone. On the right hand side of the slide, you will see that in this case there are autoantibodies to the acetylcholine receptor, which is found at the neuromuscular junction. And these autoantibodies result in another type of autoimmune disease, in this instance myasthenia gravis. The antibody inhibits binding of the ligand to the receptor, in other words it gets in the way of acetylcholine binding to its receptor. And it also has a secondary effect of causing the loss of receptors from the surface of the muscle cell. A very familiar situation to all of...

    About the Lecture

    The lecture Type 2 – Hypersensitivity by Peter Delves, PhD is from the course Hypersensitivity and Autoimmune Disease. It contains the following chapters:

    • A Closer Look on Type II Hypersensitivity
    • The Role of Antibodies in Type II Hypersensitivity
    • The Transfusion Reactions
    • Hemolytic Disease of the Fetus and Newborn

    Included Quiz Questions

    1. Autoimmune hemolytic anemia
    2. Systemic lupus erythematosus
    3. Eczema
    4. Tuberculin sensitivity
    5. Asthma
    1. Autoantibodies against the TSH receptor leads to overproduction of thyroid hormone
    2. Autoantibodies against ligand for TSH receptor leads to no stimulation of thyroid epithelial cells
    3. Overproduction of ligand leads to downregulation of TSH receptors
    4. Autoantibodies against TSH receptors leads to no production of thyroid hormone
    5. Upregulation of TSH receptor leads to autoantibodies against thyroid epithelial cells
    1. N-acetyl-fucosamine
    2. Fucose
    3. Galactose
    4. N-acetyl-galactosamine
    5. N-acetyl-glucosamine
    1. No, both A and B
    2. Both A and B, no
    3. A, B
    4. B, A
    5. O, both A and B
    1. Exposure to rhesus D during labor is required for IgG anti-rhesus antibodies to develop
    2. Antibodies can only cross the placenta in subsequent pregnancies
    3. Anti-rhesus antibodies take longer than 9 months to become active
    4. Transfer of IgG antibodies does not occur in the first pregnancy
    5. Sensitization to rhesus D occurs due injection of rhesus D antibodies to the mother 72 hours post-partum

    Author of lecture Type 2 – Hypersensitivity

     Peter Delves, PhD

    Peter Delves, PhD

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