Hipersensitivitas Tipe 3 (Immune complex-mediated Hypersensitivity), Immunology

Summary

This video explains hypersensitivity, focusing on Type 2 and Type 3 hypersensitivity reactions. Type 2 is mediated by antibodies that target specific antigens on cell surfaces, causing tissue damage. Type 3 involves immune complex deposition in various organs, leading to inflammation and tissue injury. The video further discusses the role of immune complexes in diseases like systemic lupus erythematosus (SLE), highlighting the process of complex formation, deposition, and the subsequent inflammatory response that damages body tissues, such as the skin, kidneys, and joints.

Takeaways

• 😀 Hypersensitivity Type 2 is mediated by antibodies that target specific antigens on cell surfaces, leading to tissue damage.
• 😀 Hypersensitivity Type 3 involves the formation of immune complexes between antibodies and antigens, which can deposit in various tissues and cause inflammation.
• 😀 Immune complexes in Type 3 hypersensitivity can be formed by external antigens (e.g., pathogens) or internal antigens (e.g., self-proteins).
• 😀 The deposition of immune complexes in tissues like blood vessels, kidneys, and joints can lead to inflammation and tissue damage.
• 😀 The three stages of Type 3 hypersensitivity include: 1) Formation of immune complexes, 2) Deposition in tissues, and 3) Inflammation and tissue injury.
• 😀 In Systemic Lupus Erythematosus (SLE), immune complexes form when antibodies bind to DNA fragments released from dying cells, leading to tissue damage.
• 😀 SLE is a disease where the immune system mistakenly produces antibodies against its own cells, particularly targeting nuclear material like DNA.
• 😀 The activation of the complement system and recruitment of neutrophils in Type 3 hypersensitivity causes further inflammation and tissue destruction.
• 😀 In SLE, DNA fragments are not properly cleared by immune cells, which leads to the formation of immune complexes and subsequent tissue injury.
• 😀 Type 3 hypersensitivity is a key mechanism in autoimmune diseases like SLE, where the immune system turns against the body’s own tissues, leading to chronic inflammation and damage.

Q & A

What is the primary focus of the video in the provided transcript?

The video focuses on explaining Type 2 and Type 3 hypersensitivity reactions, detailing how they function and their implications for autoimmune diseases like systemic lupus erythematosus (SLE).

What is the key difference between Type 2 and Type 3 hypersensitivity?

The main difference is that Type 2 hypersensitivity involves antibodies binding to antigens on cell surfaces, while Type 3 hypersensitivity involves immune complexes (antibody-antigen complexes) that can deposit in various tissues and cause widespread inflammation.

How do immune complexes contribute to Type 3 hypersensitivity?

In Type 3 hypersensitivity, immune complexes form when antibodies bind to antigens. These complexes deposit in tissues like blood vessels, kidneys, and joints, triggering inflammatory responses and tissue damage due to failure of immune cells to clear the complexes.

What are the three phases of Type 3 hypersensitivity?

The three phases of Type 3 hypersensitivity are: 1) Formation of immune complexes, 2) Deposition of immune complexes in various tissues, and 3) Inflammation and tissue damage due to immune system activation.

What role do neutrophils play in Type 3 hypersensitivity?

Neutrophils are recruited to the site of immune complex deposition through chemotaxis. Once there, they attempt to clear the complexes but often release enzymes that exacerbate tissue damage rather than resolving the inflammation.

What is the significance of the complement system in Type 3 hypersensitivity?

The complement system is activated when immune complexes are deposited in tissues. It acts as a chemotactic agent, signaling neutrophils to come to the site and attempt to clear the complexes, which may lead to further inflammation and tissue injury.

How does the autoimmune condition SLE relate to Type 3 hypersensitivity?

In SLE, the body generates antibodies against its own cell components, particularly nuclear material like DNA. These antibodies form immune complexes that deposit in various tissues, triggering Type 3 hypersensitivity reactions, leading to tissue damage and systemic inflammation.

What is the process of antigen formation in Type 3 hypersensitivity?

Antigens can either be exogenous (like pathogens) or endogenous (like self-DNA or glycoproteins). When these antigens interact with antibodies, immune complexes are formed, which contribute to the inflammatory response in Type 3 hypersensitivity.

Why are smaller immune complexes in Type 3 hypersensitivity more problematic?

Smaller immune complexes are harder for phagocytic cells to clear because they are not easily recognized or engulfed. This allows them to persist in circulation and deposit in tissues, triggering inflammation and further damage.

What is the role of apoptosis in the development of immune complexes in SLE?

In SLE, apoptosis (programmed cell death) can release nuclear material, including DNA fragments, into the bloodstream. These fragments can be recognized as foreign by the immune system, leading to the formation of autoantibodies against nuclear antigens and the subsequent formation of immune complexes.