Immunology: Hypersensitivity Types

Hypersensitivity reactions occur when the immune system overreacts to a usually harmless substance, like pollen or food. These reactions can be uncomfortable, damaging, and even life-threatening.

Hypersensitivity reactions involve pre-sensitization, meaning previous exposure to the allergen is required for the immune response to occur.

Types I, II, and III hypersensitivity reactions are antibody-mediated, meaning they involve antibodies like IgE, IgG, and IgM to trigger the response.

Type I hypersensitivity reactions, also known as immediate hypersensitivity, involve IgE antibodies binding to mast cells and basophils, which release histamine and other inflammatory mediators.

Type II hypersensitivity, also known as cytotoxic hypersensitivity, involves antibodies attacking cell surface antigens directly, leading to cell destruction.

Type III hypersensitivity, also known as immune-complex mediated hypersensitivity, involves antigen-antibody complexes triggering inflammation. These complexes can lodge in tissues, causing damage.

Type IV hypersensitivity, also known as delayed-type hypersensitivity, involves T lymphocytes recognizing and attacking antigens directly, and is not antibody-dependent.

The four types of hypersensitivity reactions are differentiated by the mechanisms they use to cause tissue damage and the timeline of the reaction.

A hypersensitivity reaction where the immune system overreacts to foreign antigens like pollen or food, causing immediate symptoms.

Involves antibodies targeting cell surface antigens directly, leading to cell destruction. Think of it as the body's immune system attacking its own cells.

Triggered by antigen-antibody complexes lodging in tissues, triggering inflammation. Think of them as little bombs that explode in the body.

Involves T lymphocytes recognizing and attacking antigens directly, meaning the immune system works a bit differently than in other types.

An example of Type IV hypersensitivity, the Mantoux test involves injecting purified protein derivative (PPD) and observing the reaction. Think of it as a test to see if you've encountered tuberculosis.

The immune system attacks its own tissues, resulting in diseases like SLE (lupus), autoimmune hemolytic anemia, and myasthenia gravis. Think of it as the immune system going rogue.

A severe reaction that can occur when incompatible blood types are mixed. Think of it as a major immune response to the transfusion.

An immune system reaction targeting the Rh blood type, can cause problems for babies born to Rh-negative mothers. Think of it as the mother attacking the baby's blood cells.

A mechanism where antibodies bind to target cells, triggering immune cells like NK cells to destroy them. It doesn't involve complement, but requires Fc receptors on the immune cells.

A crucial pathway of the immune system triggered by IgM or IgG antibodies. It leads to the generation of complement components like C3b and C4b, which tag target cells for destruction by phagocytes.

Antibodies that bind to blood group antigens (like A or B) causing red blood cells to be destroyed. This can lead to hemolytic anemia.

Antibodies reacting with extracellular matrix proteins can trigger complement activation and inflammation. This leads to the recruitment of neutrophils and monocytes, causing tissue damage.

Antibodies can bind to cell surface receptors, blocking their normal function. This can be either stimulatory (like Grave's disease) or inhibitory (like myasthenia gravis).

A process where phagocytes like macrophages and neutrophils engulf and destroy microorganisms that are coated with antibodies or complement components. This enhances the immune response.

Fc receptors (FcRs) are found on immune cells, specifically leukocytes, and bind to the Fc fragment of antibodies. This binding triggers various immune responses.

The process of a cell bursting or breaking apart, often due to damage caused by antibodies or complement.

An allergy is an immune response to something that does not affect most other people. It is a type of hypersensitivity reaction.

This test uses a small amount of the suspected allergen on the skin and observes for a reaction.

This blood test measures specific IgE antibodies to identify allergies.

This is a patch test that assesses contact dermatitis, where an allergen is applied to the skin and monitored for a reaction.

This test is considered the gold standard for diagnosing food allergies, where gradually increasing amounts of the suspected food are ingested and observed.

This type of sensitivity reaction involves T lymphocytes directly attacking an antigen, causing a delayed reaction.

This blood test is used to detect type IV hypersensitivity reactions, particularly to metals and chemicals.

This is an abnormal reaction of the immune system to the antibiotic drug penicillin.

A severe allergic reaction that can affect multiple body systems, potentially leading to life-threatening complications like airway closure and circulatory collapse.

An immune response triggered by the body's mistaken identification of a drug, like penicillin, as a harmful substance.

A type of immune response that involves the binding of drug allergens to IgE antibodies attached to mast cells and basophils, leading to the release of inflammatory chemicals like histamine.

A chemical released by mast cells in response to allergens, that causes allergic reactions.

An insect bite or sting that triggers a large local reaction, exceeding 5 cm in size.

An insect bite or sting that affects areas beyond the immediate bite site, with symptoms like fever, nausea or muscle aches.

A type of immune response that involves the activation of T helper 1 (TH1) cells, which play a role in inflammation, particularly in reactions to substances like formaldehyde, nickel, and poison ivy.

A skin reaction caused by direct skin exposure to a substance, like poison ivy or nickel. It's often caused by a TH1 cell-mediated response.

The main cells involved in Type IV hypersensitivity are T lymphocytes, especially CD4+ helper T cells and CD8+ cytotoxic T cells. CD4+ cells release cytokines like IFN-gamma (IFN-γ), which recruit macrophages and activate other immune cells while CD8+ cells directly kill antigen-presenting cells.

Type IV hypersensitivity reactions are characterized by delayed responses, typically occurring 24-72 hours after exposure to the triggering antigen. This delay is due to the time required for T cells to recognize the antigen, become activated, and then proliferate and differentiate into effector T cells.

Type IV hypersensitivity reactions are involved in many autoimmune diseases, inflammatory responses, and even some infections like tuberculosis and leprosy. Some common reactions caused by Type IV hypersensitivity include contact dermatitis, tuberculin reaction, and transplant rejection.

The classic Montoux test, also known as the tuberculin skin test, is a common example used to diagnose latent tuberculosis infection, which involves injecting a small amount of tuberculin (a purified protein derivative from Mycobacterium tuberculosis) into the skin. A positive reaction, a raised area of induration, indicates a delayed-type hypersensitivity response to the tuberculin indicating previous exposure to M. tuberculosis.

Contact dermatitis, a common skin allergy, is an example of Type IV hypersensitivity caused by haptens. When a sensitizing agent like poison ivy comes into contact with the skin, it triggers a strong immunological response. CD8+ T cells then specifically target and destroy cells that are expressing the hapten, resulting in the classic symptoms of redness, swelling, and itching.

In Type IV hypersensitivity, cytotoxic CD8+ T cells are directly responsible for killing cells displaying the offending antigen. These T cells release substances like granzyme and perforin, which induce apoptosis in target cells, effectively eliminating them.

Helper T (TH) cells, particularly TH1 type, play a critical role in Type IV hypersensitivity by releasing cytokines that amplify the immune response. These secreted cytokines, such as IFN-γ, TNF-α, and IL-2, recruit and activate macrophages, enhancing their ability to engulf and destroy the antigen, effectively contributing to the overall inflammatory response.