Hypersensitivity Types II, III, and IV

A type of immune reaction where antibodies mistakenly target antigens on the surface of body tissues, leading to tissue damage and inflammation.

Antibodies bind to antigens on the surface of tissue, activating complement and leading to inflammation.

A process where neutrophils bind to IgG antibodies but cannot engulf the antigen because it's fixed to tissue. This leads to the release of damaging substances from neutrophils.

A complex of proteins that forms on cell surfaces, triggering lysis (cell death).

Antibodies against RBC antigens can cause their destruction, leading to anemia.

A component of the immune system that facilitates cell lysis and inflammation, primarily triggered by antibody-antigen complexes.

A type of Type II hypersensitivity where the antibody binds to antigens on a cell's surface, leading to cell lysis or damage. This can occur when antibodies attack normal cells (autoantibodies) or foreign antigens on cells.

Antigen present on the cell surface, triggering immune responses in Type II hypersensitivity. It can be a normal part of the cell (autoantigen) or foreign antigen.

A small molecule attaching to a larger molecule, becoming antigenic and triggering an immune response. This commonly occurs in Type II hypersensitivity.

Antibodies that abnormally target self-antigens, leading to immune responses against the body's own tissues. Primarily involved in Type II hypersensitivity.

Immune responses where the antigen is present on the circulatory system or blood cells.

The most common and significant type of Type IV hypersensitivity reaction, involving the activation of macrophages by Th1 cells.

A type of T helper cell that produces IFN-gamma, leading to macrophage activation and other immune responses.

A cytokine produced by Th1 cells that activates macrophages and other immune cells.

Immune cells that engulf and destroy pathogens, enhance their ability to kill pathogens after activation by IFN-gamma.

A type of hypersensitivity reaction that occurs 24-48 hours after exposure to an antigen, characterized by delayed inflammation mediated by T cells.

A process where effector T lymphocytes travel to the site of antigen exposure after antigen presentation.

A type of cell-mediated immune response where T cells directly kill target cells

A type of immune reaction where antibodies mistakenly target antigens on the surface of body tissues, leading to tissue damage and inflammation.

When antibodies against RBC antigens bind to the surface of red blood cells, leading to their destruction.

The process where neutrophils adhere to antibody-coated antigens but cannot engulf them due to their attachment to a surface, leading to the release of damaging enzymes.

A type of hypersensitivity reaction where soluble antigens form immune complexes that deposit in blood vessels, triggering inflammation, tissue damage, and vasculitis.

Antigen-antibody complexes that form in the blood and can vary in size, with small complexes being most crucial in type III hypersensitivity.

The process where immune complexes deposit in blood vessels, activating complement, leading to inflammation and vessel damage.

A series of proteins that form a pore on the cell membrane, leading to cell lysis (destruction).

Inflammation of blood vessels, often caused by the deposition of immune complexes in Type III hypersensitivity.

T cells migrate from the bloodstream to the site of infection, a process guided by chemokines and selectins.

Chemokines, such as C3a, C5a, attract T cells to the site of infection.

Activated T cells undergo significant changes in receptor expression, leading to a decrease in CCR7 and an increase in S1P receptor expression.

Selectins, such as P-selectin, E-selectin, and L-selectin, guide T cell movement by facilitating their interaction with the blood vessel walls.

T cell migration from blood vessels to tissues involves a multistep process involving rolling, adhesion, and transmigration across the endothelium.

T cell migration contributes to inflammation by recruiting immune cells, such as macrophages, to the site of infection.

The delay in the immune response is due to the time required for T cells to migrate to the site of infection.

T cells are responsible for initiating the immune response at the infection site, leading to localized inflammation and tissue damage.

Organisms like Mycobacterium tuberculosis (TB) and leprosy bacteria can resist destruction by macrophages, leading to the formation of giant cells and granulomas in the body.

Superantigens, like those involved in toxic shock syndrome, cause a strong immune response by activating many T cells non-specifically. This leads to the release of large amounts of inflammatory cytokines, causing a severe immune response similar to septic shock.

A skin prick test involves pricking the skin with a small amount of allergen to see if there is a reaction.

A skin scratch test involves making a deep scratch on the skin with a blunt lancet to introduce the allergen.

A skin scrape test involves scraping the superficial layer of the epidermis to assess the presence of allergens.

An intradermal test involves injecting a small amount of allergen under the skin with a syringe.

A patch test involves applying a patch containing the allergen to the skin and observing for a reaction after a designated period.

Photopatch testing is a modification of the patch test in which, after one day, the patch is removed, and the skin is exposed to UV light. This is especially helpful for assessing photoallergic reactions.