Type IV Hypersensitivity (Described Concisely)

Summary

This video explains the mechanisms behind Type 4 hypersensitivity reactions, focusing on T-cell mediated responses, in contrast to the antibody-driven responses of Types 1, 2, and 3. The script uses the example of poison ivy exposure to demonstrate how T helper cells and cytotoxic T cells are activated to cause tissue damage and inflammation. Other examples include tuberculosis skin tests, metal allergies, and autoimmune diseases like Type 1 diabetes and rheumatoid arthritis. The video provides a thorough explanation of how cytotoxic T cells target cells directly and initiate apoptosis, leading to various clinical manifestations.

Takeaways

• 😀 Type 4 hypersensitivity is a T-cell mediated immune response, unlike types 1, 2, and 3, which are antibody-mediated.
• 😀 Type 4 hypersensitivity involves T-helper cells and/or cytotoxic T-cells, and is not a humoral-mediated response.
• 😀 In the case of poison ivy, urushiol binds to skin proteins, altering them and triggering the immune response, recognized as foreign by the immune system.
• 😀 The immune system processes these altered proteins with the help of antigen presenting cells (APCs), which present the proteins to naive T-helper cells.
• 😀 T-helper cells differentiate into Th1 or Th17 cells based on cytokines released by APCs, leading to different immune responses.
• 😀 Th1 cells release IFN-gamma, activating macrophages, which cause tissue damage by phagocytosis and release of reactive oxygen species.
• 😀 Th17 cells release IL-17 to activate neutrophils, causing inflammation similar to the Th1 response.
• 😀 Type 4 hypersensitivity reactions take time (24-72 hours) to develop, as T-cells need to be activated and recruited to the site of reaction.
• 😀 The tuberculosis (TB) skin test is an example of type 4 hypersensitivity, where injected proteins cause a delayed immune response in previously exposed individuals.
• 😀 Type 4 hypersensitivity also includes conditions like metal allergies, latex contact dermatitis, and autoimmune diseases like type 1 diabetes and rheumatoid arthritis, where cytotoxic T-cells directly attack target cells.
• 😀 Cytotoxic T-cells use perforin and granzymes or Fas ligand mechanisms to induce apoptosis (programmed cell death) of the targeted cells, leading to tissue damage.

Q & A

What distinguishes Type 4 hypersensitivity from Types 1, 2, and 3 hypersensitivity?

Type 4 hypersensitivity is T-cell mediated and does not involve antibodies, unlike Types 1, 2, and 3, which are humoral and involve antibodies in their immune responses.

What role do T-helper cells play in Type 4 hypersensitivity?

T-helper cells are activated by antigen-presenting cells (APCs), and depending on the cytokines released, they differentiate into either Th1 or Th17 cells, which mediate the immune response and inflammation.

What is the mechanism behind the immune response to poison ivy in Type 4 hypersensitivity?

Urushiol in poison ivy binds to skin proteins, altering them. The immune system recognizes these altered proteins as foreign, and APCs present them to naive T-helper cells, triggering a T-cell mediated response.

What is the typical timeline for the development of symptoms in Type 4 hypersensitivity?

Symptoms of Type 4 hypersensitivity, such as a rash from poison ivy, typically appear 24 to 72 hours after exposure.

How do Th1 cells contribute to the inflammatory response in Type 4 hypersensitivity?

Th1 cells release IFN-γ, which activates macrophages. These macrophages recruit leukocytes and cause tissue damage through phagocytosis, the release of reactive oxygen species, and toxic lysosomal enzymes.

What role do Th17 cells play in Type 4 hypersensitivity?

Th17 cells release IL-17, which activates neutrophils and leads to similar inflammatory actions as macrophages, contributing to tissue damage.

How does the tuberculosis (TB) skin test relate to Type 4 hypersensitivity?

The TB skin test involves injecting Mycobacterium tuberculosis proteins into the skin. If the person has been previously infected, their immune system will mount a Type 4 hypersensitivity response, causing a raised lesion at the injection site.

What are some other examples of Type 4 hypersensitivity reactions besides poison ivy and TB skin tests?

Other examples include metal allergies (e.g., nickel), contact dermatitis from latex, and autoimmune diseases where cytotoxic T cells attack specific tissues, such as in Type 1 diabetes and rheumatoid arthritis.

How do cytotoxic T cells contribute to Type 4 hypersensitivity in autoimmune diseases?

Cytotoxic T cells target specific cells, such as insulin-producing beta cells in Type 1 diabetes or joint tissue in rheumatoid arthritis, and induce cell death through the release of granzymes and perforins.

What are granzymes and perforins, and how do they function in Type 4 hypersensitivity?

Granzymes are proteases released by cytotoxic T cells that induce apoptosis (programmed cell death) in target cells. Perforins create pores in the target cell membrane, allowing granzymes to enter and cause cell death.