Humoral Immune Response II Quiz

Antibodies are grouped into 5 main types: IgG, IgA, IgM, IgE, and IgD. Each type has a specific role in the immune response.

Antibodies bind to pathogens and toxins, blocking their harmful effects and activating other immune cells to eliminate them.

NK cells use antibodies to identify and destroy infected cells.

A group of proteins that work with antibodies to destroy pathogens.

The immune response that uses antibodies to fight infection.

Antibodies have a specific structure for various functions.

Complement pathway activated by antibodies, specifically IgG.

Maternal antibodies protect a newborn by crossing the placenta.

Antibodies have unique shapes for targeting specific invaders (viruses, bacteria, etc).

Antibodies block microbes from entering cells.

The initial step of infection, where microbes bind to host cells.

A molecule on the surface of a microbe that allows it to attach to host cells.

Antibodies blocking a microbe's ability to bind to host cells or toxins.

Harmful toxins produced by bacteria, often lethal.

Harmful substances, produced by bacteria or other organisms, causing harm or disease

Antibodies that neutralize toxins

The ability of a microbe to attach to specific cells of a specific host.

Preventing toxins from doing harm by blocking their interactions with target cells

Leishmania infects macrophages by adhering, entering, multiplying, then rupturing the cell, spreading to other cells.

Antibodies block toxins from binding to cell receptors, preventing their harmful effects.

Antibodies coat microbes, enhancing phagocytosis (ingestion) by immune cells.

Molecules that coat microbes to enhance phagocytosis.

Antigen-antibody complexes trigger a complement system cascade generating C3b (opsonin)

Microbial presence directly triggers the complement system generating C3b, facilitating phagocytosis

High-affinity receptor for IgG Fc regions that help phagocytic cells bind IgG-coated microbes.

Ingestion and destruction of microbes by phagocytic cells.

The process by which parasites are killed by eosinophils, leading to lysis (cell breakdown) and eventual elimination from the body.

Eosinophils are a type of white blood cell that contain toxic substances that kill parasitic worms. They are responsible for the death of parasites in the body.

The process by which complement proteins work in a cascade to identify and destroy pathogens. It involves processes like opsonization, cytolysis, and inflammation.

A complex of complement proteins that forms holes in the membranes of pathogens, leading to their destruction. It is a key part of the complement system's defense.

Complement components like C3a and C5a trigger inflammation by attracting neutrophils to the site of infection. This helps to fight off the invading pathogens.

Neutrophils, a type of white blood cell, are attracted to the site of infection by complement byproducts, like C3a and C5a. They help to fight off infection by engulfing pathogens and releasing inflammatory substances.

Antibody-dependent cell-mediated cytotoxicity (ADCC) is a process where NK cells use antibodies to target and destroy infected or cancerous cells.

An antibody binds to an antigen on the surface of a target cell. NK cells, with Fc receptors that recognize the antibody's Fc region, bind to the antibody. This triggers the NK cell to release cytotoxic granules, like perforins and granzymes, which destroy the target cell.

IgG antibodies are most commonly used in ADCC because NK cells have a high affinity for their Fc region.

Eosinophils are white blood cells that primarily fight parasitic infections, especially helminths (worms).

Th2 cells release IL-5, which activates eosinophils. This enhances their ability to kill parasites.

Eosinophils have receptors called FcεRI that bind to IgE antibodies, which are attached to the surface of parasites.

Eosinophils release toxic substances, like major basic protein (MBP), from their granules. These substances damage parasites and kill them.

IgE antibodies bind to antigens on parasites, making them attractive targets for eosinophils, which have FcεRI receptors to recognize the IgE.