M2: Immune Hypersensitivity

Immune hypersensitivity

An abnormal or excessive immune reaction to an antigen, causing host tissue damage

What are the 3 consequences of immune hypersensitivity?

Allergy, autoimmunity, alloimmunity

Allergy

The immune system overreacts to innocuous environmental substances, such as pollen, dust mites, or certain foods.

• this triggers a rapid release of inflammatory mediators, leading to symptoms like sneezing, itching, and in severe cases, anaphylaxis

Autoimmunity

The immune system loses its ability to distinguish “self” from “non-self”, leading to an immune attack on the body’s own cells and tissues.

• ex: rheumatoid arthritis, type 1 diabetes, and multiple sclerosis

Alloimmunity

Occurs when the immune system of one individual reacts against antigens from another individual

• when a recipient’s immune system attacks the transplanted organ

• also plays a role in certain complications of pregnancy such as hemolytic disease of the newborn, where maternal antibodies target fetal antigens

Sensitization

The first encounter with an antigen (allergen or autoantigen) triggers an immune response

• leads to the activation of T and B lymphocytes, resulting in the generation of memory cells and antibodies specific to that antigen.

• This initial exposure “primes” the immune system for a subsequent encounter with the same antigen

Activation

Upon re-exposure to the antigen, memory cells and antibodies rapidly recognize and bind to it.

• this triggers a cascade of immune events, leading to the activation of various hypersensitivity mechanisms such as inflammation

Tissue damage

This phase involves the actual tissue damage and inflammation cause by the activated immune components

Type I hypersensitivity

Triggered by the cross-linking of IgE bound to mast cells and basophils

• inflammatory mediators cause vasodilation, increased vascular permeability, smooth muscle contraction, and mucus secretion

Type II hypersensitivity

Antibodies bind to cell surface antigens, leading to complement activation and cell destruction

• Complement activation leads to cell lysis; phagocytes engulf and destroy antibody-coated cells; NK cells stimulate apoptosis in antibody-coated cells

Type III hypersensitivity

Immune complexes form and deposit in tissues, activating complement and attracting neutrophils

• Complement activation and neutrophil recruitment result in inflammation and tissue damage

Type IV hypersensitivity

T cells are activated and either activate macrophages or directly kill target cells

• macrophage and cytotoxic T cell activity lead to tissue inflammation and damage

Immediate hypersensitivity reactions

Typically occur within minutes to hours after antigen re-exposure

• this response is primarily observed in type I, II, and III which are mediated by IgE, IgG, and IgM

• Can involve anaphylaxis

Delayed hypersensitivity reactions

May take 12-72 hours to manifest after antigen re-exposure

• this response is characteristic of type IV hypersensitivity reactions, which are primarily mediated by T cells rather than antibodies

• not associated with anaphylaxis