Types of Immune Response: Hyperreactivity Types III & IV

A type of hypersensitivity reaction where immune complexes form and deposit in tissues, leading to inflammation and tissue damage. This reaction is mediated by IgG and IgM antibodies against soluble antigens.

A self-limited illness occurring 6-15 days after exposure to foreign serum, characterized by fever, rash, joint pain, blood vessel inflammation, and kidney inflammation.

A localized, immune-mediated blood vessel inflammation resulting in tissue death. Triggered by injecting an antigen into a sensitized individual.

Inflammation and damage to blood vessels due to immune complex deposition, leading to characteristic microscopic features.

A type of cell death characterized by a granular, lumpy appearance, often associated with immune complex deposition.

A type of hypersensitivity reaction involving T cells, macrophages, and cytokines, leading to cell destruction and delayed inflammation.

Inflammation that occurs 24 hours after exposure to an antigen, peaking after 2-3 days and lasting for several days.

Cells that present antigens to T cells, initiating the immune response in Type IV hypersensitivity.

Immune cells that engulf and destroy pathogens and cellular debris, playing a crucial role in Type IV hypersensitivity.

Small proteins that act as messengers in the immune system, contributing to the inflammatory response in Type IV hypersensitivity.

A type of immune reaction that targets the body's own tissues, often mediated by Type III hypersensitivity.

Type IV hypersensitivity is a cell-mediated immune response, unlike the antibody-mediated reactions in types I-III. It involves a delayed reaction, meaning the immune response takes time to develop.

CD4+ T-helper cells (Th1/Th17) are activated by persistent, non-degradable antigens. This triggers the release of inflammatory mediators like IFN-gamma, which, in turn, transforms macrophages into epithelioid cells. This process leads to granuloma formation.

The Mantoux test, also known as the tuberculin skin test, utilizes a purified mycobacterial antigen. When injected into a previously immunized individual, it triggers a delayed-type hypersensitivity reaction detectable within 24-48 hours. This reaction is a diagnostic tool for tuberculosis.

Granuloma formation is a common outcome of Type IV hypersensitivity. It occurs when macrophages are unable to completely eliminate intracellular pathogens, leading to persistent T cell activation. These activated T cells then accumulate around the infected cells, forming the granuloma.

Allergic contact dermatitis is a type IV hypersensitivity reaction triggered by contact with certain chemicals, metals, or medications. It causes inflammation, rash, and blisters due to epidermal necrosis.

In Type IV hypersensitivity, CD8+ cytotoxic T lymphocytes (CTLs) play a crucial role. These cells are activated by antigens presented on infected or abnormal cells and directly kill these cells through apoptosis.

Type 1 diabetes, a chronic autoimmune condition, is caused by the destruction of pancreatic islet cells. Cytotoxic T cells specifically target these cells, leading to insulin deficiency.

Graft-versus-host disease (GvHD) occurs when immune cells from a donor (graft) attack the recipient's tissues. This is a type IV hypersensitivity reaction where donor T cells recognize recipient antigens as foreign and initiate an immune response.

Chronic transplant rejection is another example of type IV hypersensitivity. It occurs when the recipient's immune system gradually attacks the transplanted organ, leading to its dysfunction over time.

Type IV hypersensitivity is distinct from the other types (I-III) because it's a cell-mediated response rather than antibody-mediated. It's also delayed because the immune reaction takes time to develop.