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Type I hypersensitivity
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Rheumatic heart disease
Type II hypersensitivity
Systemic lupus erythematosus
Type III hypersensitivity
Type IV hypersensitivity
Common variable immunodeficiency
Hyperimmunoglobulin E syndrome
IgG subclass deficiency
Isolated primary immunoglobulin M deficiency
Selective immunoglobulin A deficiency
Adenosine deaminase deficiency
Hyper IgM syndrome
Severe combined immunodeficiency
Cytomegalovirus infection after transplant (NORD)
Post-transplant lymphoproliferative disorders (NORD)
Chronic granulomatous disease
Leukocyte adhesion deficiency
Blood transfusion reactions and transplant rejection: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
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Hypersensitivity Type II
type II hypersensitivity p. 110
type II hypersensitivity reactions p. 110
in type II hypersensitivity p. 110
blood transfusions p. 112
organ transplants p. 117
rheumatic fever p. 318
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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