Antibody-Dependent Cell-Mediated Cytotoxicity: Type II Hypersensitivity Reaction

Summary

Type II hypersensitivity reactions involve the immune system attacking its own cells through antibody-dependent cell-mediated cytotoxicity (ADCC). This process includes complement system activation, neutrophil and macrophage involvement, and natural killer (NK) cell-mediated cell death. These immune responses lead to cell lysis, inflammation, and tissue damage. In autoimmune diseases, antibodies can disrupt normal cell function by blocking or activating cell surface receptors, causing severe physiological consequences. Understanding these mechanisms is crucial in comprehending the underlying causes of autoimmune disorders.

Takeaways

• 😀 Type II hypersensitivity involves the immune system attacking the body's own cells through antibody-mediated processes.
• 😀 In this response, antibodies are directed at antigens present on the surface of cells or within connective tissue.
• 😀 The complement system plays a central role in triggering immune responses, leading to further activation of immune cells.
• 😀 Complement activation results in a cascade that attracts neutrophils, causing inflammation and cell damage.
• 😀 Neutrophils, upon activation, generate substances like reactive oxygen species that contribute to cell death.
• 😀 Opsonization is a key process where complement proteins mark cells for recognition by phagocytes like macrophages.
• 😀 Macrophages engulf and break down target cells marked by antibodies, contributing to the immune response.
• 😀 The membrane attack complex (MAC) is formed during complement activation, leading to target cell lysis.
• 😀 Natural killer (NK) cells are involved in Type II hypersensitivity by recognizing antibody-coated cells and releasing perforin and granzymes.
• 😀 NK cells release perforin to create pores in the target cell membrane, inducing cell lysis, while granzymes trigger apoptosis.
• 😀 Type II hypersensitivity can lead to autoimmune diseases where antibodies disrupt normal cell receptor functions, either by blocking or activating them.

Q & A

What is Type II hypersensitivity?

Type II hypersensitivity is an immune response where the body’s immune system mistakenly targets its own cells due to the presence of specific antibodies. This leads to immune-mediated cell damage, including processes like cell lysis, phagocytosis, and apoptosis.

How does antibody-dependent cell-mediated cytotoxicity (ADCC) occur in Type II hypersensitivity?

ADCC occurs when antibodies bind to antigens on the surface of cells. This binding activates the immune system, leading to cell damage through complement activation, recruitment of immune cells like neutrophils, and activation of natural killer (NK) cells, ultimately causing cell death.

What role do antibodies play in Type II hypersensitivity reactions?

In Type II hypersensitivity, antibodies, particularly IgG, bind to antigens on the surface of the body's own cells or connective tissues. This initiates immune responses that result in cell damage, inflammation, and destruction through various immune mechanisms.

What is the complement system, and how does it contribute to Type II hypersensitivity?

The complement system is a group of plasma proteins that, when activated, trigger a cascade of immune responses. In Type II hypersensitivity, complement activation leads to inflammation, recruitment of immune cells like neutrophils, and the destruction of cells via cell lysis.

How do neutrophils contribute to the immune response in Type II hypersensitivity?

Neutrophils play a key role by recognizing antibodies bound to antigens via Fc receptors. Once bound, neutrophils release reactive oxygen species and other substances that cause inflammation and damage to the target cells.

What is opsonization, and how does it affect the immune response in Type II hypersensitivity?

Opsonization is the process by which complement proteins mark target cells for destruction. These marked cells are then recognized and engulfed by phagocytes, particularly macrophages, which break down the damaged cells.

What is the role of natural killer (NK) cells in Type II hypersensitivity?

NK cells are involved in recognizing antibody-coated cells. They bind to the antibodies through Fc receptors, release perforin to induce cell lysis, and also release granzymes to trigger apoptosis, leading to the destruction of the target cells.

How does the complement system cause cell lysis in Type II hypersensitivity?

The complement system leads to the formation of the membrane attack complex (MAC), which inserts into the target cell’s plasma membrane, causing an influx of extracellular fluid. This results in the swelling and eventual lysis of the cell.

Can antibodies in Type II hypersensitivity cause disruptions to normal cell function?

Yes, antibodies in Type II hypersensitivity can either block cell surface receptors, preventing normal signaling, or activate them abnormally, leading to dysfunction. Both scenarios can have severe physiological consequences.

What are the general outcomes of a Type II hypersensitivity reaction?

The primary outcome of a Type II hypersensitivity reaction is the death of target cells, which can be caused by complement-mediated lysis, phagocytosis, or NK cell-induced apoptosis. This leads to inflammation due to the release of cellular contents.