Type II hypersensitivity

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Type II hypersensitivity


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USMLE® Step 1 questions

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Type II hypersensitivity

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USMLE® Step 1 style questions USMLE

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A 50-year-old man is diagnosed with myasthenia gravis, a chronic autoimmune condition characterized as a type II hypersensitivity reaction. Which of the following best describes the underlying mechanism of this disease?

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Bullous pemphigoid p. 487, 493

type II hypersensitivity p. 110

Erythroblastosis fetalis p. 416

type II hypersensitivity p. 110

Goodpasture syndrome p. 48, 620

type II hypersensitivity reactions p. 110

Graves disease

type II hypersensitivity p. 110

Idiopathic thrombocytopenic purpura (ITP)

type II hypersensitivity reactions p. 110

Membrane attack complex (MAC) p. 102

in type II hypersensitivity p. 110

Myasthenia gravis p. 484

type II hypersensitivity p. 110

Pemphigus vulgaris p. 493

type II hypersensitivity p. 110

Rheumatic fever p. 321

type II hypersensitivity p. 110

Type II hypersensitivity p. 110

blood transfusions p. 112

organ transplants p. 117

Type II hypersensitivity reactions

rheumatic fever p. 320

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Having a hypersensitivity means that the immune system is reacting to something in a way that damages the body rather than protecting it.

There are four different types of hypersensitivities, and the second type or type II hypersensitivity is sometimes called cytotoxic hypersensitivity because a lot of disorders caused by this hypersensitivity involve antibody mediated destruction of healthy cells.

These disorders tend to be tissue specific meaning that the antibodies are generally specific to one type of tissue or organ.

There are other antibody-mediated hypersensitivities that are systemic, and these are generally Type III hypersensitivities.

Our immune system is setup to fight anything that is considered “non-self” right? Anything that’s not “self”, or you.

This works in large part because of a process called central tolerance which is when developing immune cells that are self-reactive get destroyed or inactivated, whereas immune cells that aren’t are allowed to survive.

This happens while they are still in their primary lymphoid organs, which is the thymus for T cells and the bone marrow for B cells.

This process, though, is not perfect and some self-reactive B and T cells will escape.

These escaped self-reactive cells can then attack healthy tissue and result in autoimmune disease.

In type II hypersensitivity these escaped self-reactive B cells become activated and produce IgM or, with the help of CD4 positive T helper cells, IgG antibodies that attach to antigens on host cells.

There are two type of antigens involved with type II hypersensitivity: intrinsic meaning an antigen the host cell normally makes or extrinsic which is an antigen from an infection or even some medications, like penicillin that gets attached to the host cell.


Type II hypersensitivity is a type of immune response in which the immune system attacks the body's own cells or tissues. Type II hypersensitivity is mediated by antibodies, such as IgG and IgM, directed against antigens on host cells, which cause cell and tissue destruction by complement activation or antibody-dependent cell-mediated cytotoxicity. Examples of Type II hypersensitivity reactions include blood transfusion reactions, erythroblastosis fetalis, and autoimmune hemolytic anemia. Treatment options may include avoiding the tigger, and immunosuppressive medications such as systemic glucocorticoids.


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