Type III hypersensitivity (immune complex mediated) - causes, symptoms & pathology

Summary

This video delves into type III hypersensitivity reactions, focusing on the role of immune complexes in causing inflammation and tissue damage. It explains how these immune complexes, formed when antibodies bind to soluble antigens, can lead to diseases like lupus and serum sickness. Key processes such as B cell activation, antigen-antibody binding, and complement system activation are explored. The video highlights how immune complexes cause vasculitis, glomerulonephritis, and arthritis, and emphasizes the difference between type III and type II hypersensitivity reactions, offering insights into disease progression and immune responses.

Takeaways

• 😀 Type III hypersensitivity occurs when antigen-antibody complexes deposit in blood vessel walls, causing inflammation and tissue damage.
• 😀 Immune complexes consist of two parts: the antigen and the antibody, with antibodies being produced by plasma cells (mature B cells).
• 😀 B cells initially produce IgM antibodies, which then undergo class switching to IgG in response to activation by T helper cells.
• 😀 Antibodies are specific to antigens, which can be soluble in the blood or bound to cell surfaces. Type III hypersensitivity involves immune complexes with soluble antigens.
• 😀 A key distinction between Type II and Type III hypersensitivities is that Type II involves antibodies binding to cell surface antigens, whereas Type III involves soluble antigens forming immune complexes.
• 😀 An example of Type III hypersensitivity is systemic lupus erythematosus (lupus), where IgG antibodies target DNA and nucleoproteins (self-antigens).
• 😀 Normally, the immune system avoids attacking self-antigens through tolerance, but in lupus, self-reactive cells may escape and cause an autoimmune response.
• 😀 In lupus, IgG antibodies bind to DNA autoantigens, forming immune complexes that can lead to inflammation and tissue damage.
• 😀 Immune complexes in Type III hypersensitivity activate the complement system, which increases vascular permeability and recruits neutrophils, leading to tissue inflammation and damage.
• 😀 Clinical symptoms in Type III hypersensitivity are linked to the tissue where immune complexes are deposited (e.g., kidneys causing glomerulonephritis, joints causing arthritis), not where the immune complexes are produced.
• 😀 Serum sickness, another example of Type III hypersensitivity, occurs when the body creates antibodies against foreign antigens (e.g., anti-venom antibodies), leading to immune complex formation and subsequent vasculitis and tissue necrosis.

Q & A

What is hypersensitivity, and how does it differ from the immune system's normal function?

Hypersensitivity occurs when the immune system reacts to something in a way that ends up damaging the body, instead of protecting it. Normally, the immune system defends against foreign invaders, but in hypersensitivity, this defense turns into a harmful reaction.

What are the four types of hypersensitivity, and which one is discussed in the video?

There are four types of hypersensitivity: type I (immediate), type II (cytotoxic), type III (immune complex), and type IV (delayed). The video specifically discusses type III hypersensitivity, which involves the deposition of antigen-antibody complexes in blood vessel walls.

How are immune complexes formed in type III hypersensitivity reactions?

Immune complexes are formed when antibodies bind to soluble antigens. These complexes can deposit in various tissues, including blood vessel walls, causing inflammation and tissue damage.

What role do B cells play in type III hypersensitivity reactions?

In type III hypersensitivity, B cells are activated by T helper cells and undergo class switching to produce IgG antibodies that target specific antigens, forming immune complexes.

What is the difference between immune complexes in type II and type III hypersensitivity?

In type II hypersensitivity, antibodies bind directly to antigens on cell surfaces, whereas in type III hypersensitivity, immune complexes are formed when antibodies bind to soluble antigens.

How does lupus relate to type III hypersensitivity?

Lupus is an autoimmune disease in which IgG antibodies target self-antigens, such as DNA and nucleoproteins, leading to the formation of immune complexes that deposit in tissues and cause inflammation and damage.

What happens when immune complexes are deposited in the basement membrane of blood vessels?

Once immune complexes deposit in the basement membrane of blood vessels, they activate the complement system, leading to increased vascular permeability, fluid leakage, and recruitment of immune cells like neutrophils, which cause inflammation and tissue damage.

What is the role of the complement system in type III hypersensitivity?

The complement system is activated when immune complexes bind to complement proteins. This activation leads to the release of anaphylatoxins (such as C3a, C4a, and C5a), which increase vascular permeability and recruit immune cells, contributing to inflammation and tissue damage.

What are some clinical manifestations of type III hypersensitivity?

Clinical symptoms of type III hypersensitivity depend on where the immune complexes are deposited. Common manifestations include glomerulonephritis (inflammation of the kidney) and arthritis (inflammation of the joints).

How does serum sickness relate to type III hypersensitivity?

Serum sickness is an example of type III hypersensitivity where the body reacts to foreign serum (such as anti-venom) by forming immune complexes between the foreign antibodies and the patient's own immune system, leading to vasculitis and tissue necrosis.