The links below take you to some additional resources on the immune system.
This chapter discusses several different mechanisms used to defend the body against pathogens and toxic chemicals. The first line of defense consists of mechanisms that prevent harmful substances from entering the body.
If the barriers become breached and foreign materials enter the body, a number of mechanisms act to prevent them from doing harm. Innate immunity refers to nonspecific mechanisms that are generally effective against a variety of infections. It constitutes a second line of defense. The effectiveness of innate immunity is not enhanced by exposure to infectious agents.
The detection of foreign particles involves the use of receptors. A reaction is triggered when foreign particles bind to a receptor. Receptors used in the innate immune response are able to bind to molecules that are common in pathogens but are not found in the animal's body.
A third line of defense, called adaptive immunity, consists of mechanisms that are specific for one type of infection. Adaptive immunity is generally acquired after exposure to the infecting particles or cells and is therefore slower than innate immunity.
Receptors used in adaptive immunity are specific. They often function for a specific type of molecule which may be found only in a specific kind of infection. Due to their specificity, a large variety of these receptors are needed in order to respond to a large number of possible infective agents. When one specific kind of these receptors binds to molecules, the resulting reactions produce many more of the same kind of receptor. Thus, exposure to an infective agent increases the number of receptors capable of binding to that agent.
Innate immunity is found in all animals. Adaptive immunity is found only in vertebrates.
The skin and epithelial tissue covering the body's exterior and interior surfaces are the main barrier preventing the entry of foreign organisms and particles. The cells of these surface tissues are linked by tight junctions which prevents the passage of materials between the cells. These cells are dead and contain a tough, waterproofing protein called keratin.
Dryness prevents many microbes from growing on the skin.
The low pH of skin oils, earwax and sweat glands weaken or kill bacteria.
Mucus, produced by mucous membranes, traps microorganisms and other small particles. Cilia lining the respiratory tract sweep mucus and trapped particles to the pharynx where they are swallowed.
The low pH of the stomach kills microorganisms that are swallowed.
Tears wash the eyes.
Earwax protects the ears.
Saliva helps clean teeth, preventing dental caries.
Urine flow prevents colonization of the urinary tract.
The low pH of the vagina kills or inhibits many kinds of microorganisms. Vaginal secretions move microorganisms out of the reproductive tract.
Lysozyme is found in tears, saliva, mucus, tissue fluids, and perspiration. It inhibits many kinds of bacteria by breaking down their cell walls.
The normal bacterial colonists of the skin, gut, and vagina prevent harmful microorganisms from colonizing the areas.
Innate Cellular Responses
A variety of white blood cells (leukocyes) function in both innate and adaptive immunity.
Some leukocytes are phagocytic (capable of phagocytosis). They contain toll-like receptors that are able to recognize certain patterns of molecules typically found in pathogens but not in the host. These are called pathogen-associataed molecular patterns. Some examples are lipopolysaccharides in the outer membrane of gram negative bacteria, peptidoglycan, flagellin, DNA and RNA. Materials that are identified by this method are then phagocytized.
Particles bound to the toll-like receptors of phagocytes are phagocyted. Binding stimulates the phagocyte to release cytokines, which attract more phagocytes to the area.
Phagocytes are attracted by chemical signals present in damaged or infected tissue and by cytokines and peptides produced by the compliment system.
During phagocytosis, the foreign particle is engulfed by the phagocyte and brought into the cell within a vesicle (a phagosome). The vesicle containing the foreign material then fuses with a lysosome containing digestive enzymes that are capable of destroying the contents of the vesicle. Next, the vesicle containing the remnants of digestion fuses with the plasma membrane, emptying its contents to the outside.
Foreign cells and particles are more likely to be phagocytized if they have antibodies or compliment proteins attached to their surface. The attachment of these molecules is called opsonization and is discussed later.
Neutrophils are found in the blood. They are attracted to damaged or infected tissue by chemical signals.
Macrophages are found in the blood and also in the tissues.
Dendritic cells are found on surfaces that are exposed to the environment. When activated, they move to the lymph nodes and interact with B and T lymphocytes.
Natural Killer Cells
Natural killer cells are able to recognize and then kill virus-infected cells and cancer cells because they have fewer MHC class I self antigens (discussed below) on their surface than normal body cells. They release perforins, proteins that insert into the plasma membrane of the target cell, creating pores that cause it to lyse. Natural killer cells also release enzymes called granzymes which cause apoptosis.
The inflammatory reaction is a local response to injury or infection.
Damaged tissue stimulates mast cells to release histamine which causes an increase in blood vessel diameter (vasodilation) and increased permeability of the blood vessels. This brings more blood flow to the area including more infection-fighting leukocytes (white blood cells) such as monocytes and neutrophils.
Inflammation occurs when fluids and infection-fighting cells leak from the blood vessels into the tissues. The swelling and redness associated with inflammation is due to increased blood flow to the area and to fluid leaking from the blood vessels into the tissues.
Macrophages are activated when their toll-like receptors bind to foreign molecules. These activated macrophages release signaling molecules called cytokines which, like histamine, cause vasodilation and increased permeability of the blood vessels. Cytokines released by macrophages attract neutrophils and monocytes to the area. Within the tissues, monocytes differentiate into macrophages.
The toll-like receptors of neutrophils and macrophages enable them to identify foreign material which they phagocytize.
Bacteria may release chemicals that kill leukocytes. In addition, neutrophils are often killed as a result of chemical processes used to kill pathogens after phagocytosis. Pus is a substance that contains a large number of dead leukocytes, particularly neutrophils, and other debris that remains at the infection or damage site.
Some pathogenic organisms are too large to be phagocytized. Instead, these organisms are killed by chemicals released by macrophages, neutrophils, and eosinophils.
The Complement System
The complement system consists of a number of different proteins that help defend the body when they are activated. It is called complement because it enhances (complements) other immune responses such as the inflammatory reaction (an innate response discussed above) and the antibody-mediated response (an adaptive response discussed later).
Compliment proteins function in innate immunity when they are activated by molecules on the surface of microorganisms. Each activated complement protein activates many others so that a large number of active proteins are produced.
Compliment proteins are also activated when they attach to antibodies that have attached to antigens.
Some activated complement proteins form membrane attack complexes which produce holes in bacterial cell membranes. The holes disrupt the osmotic balance by allowing salts and fluids to enter, rupturing the cell.
Activated compliment proteins also stimulate mast cells, promoting the release of histamine and enhancing the inflammation reaction discussed above.
Interferons are proteins produced by virus-infected animal cells that stimulate themselves and other nearby cells to produce substances that interfere with viral replication. Interferons may also activate natural killer cells.
Lysozyme is an enzyme capable of breaking down the cell walls of gram-positive bacteria. It is found in sweat, tears, saliva, nasal secretions, and tissue fluids.
Epithelial tissues, along with neutrophils, produce chemical substances called defensins that attach to microbial cell membranes forming pores in the membrane, thus killing the microorganism.
Antigens are usually foreign molecules that have entered the body. The body is able to recognize that they are foreign because it has antigen receptors that are able to bind to specific antigens.
Antigen receptors are able to attach to a portion of the antigen because the shape matches. The portion of the antigen that matches the shape of the receptor is called an epitope.
The body does not produce antigen receptors that bind to its own (self) antigens. Therefore particles that are bound to antigen receptors are foreign.
The two kinds of immunity discussed in this section require that the body be able to identify its own cells (self) from foreign particles and foreign cells. When antigens are discovered, they need to be displayed so that other immune cells can be activated and then remove the foreign particles. The lymphocytes involved also need to be able to distinguish which self cells have been infected so that the infected cells can be destroyed.
Body cells contain proteins on their surface called MHC (major histocompatability complex) proteins. Every person has unique MHC proteins. When a body cell is infected, the infected cell will attach antigens from the pathogen to class I MHC proteins and then move the MHC-antigen complex to the surface of the cell. This marks the cell as being infected and certain other lymphocytes that can see the MHC-antigen complex will destroy the infected cell, preventing the infection from spreading.
The class I MHC proteins attached to the cell in the drawing below indicate that it is one of the body's own cells. The antigen fragments attached to the class I MHC proteins indicate that the cell is infected. Antigen fragments which are attached to class I MHC proteins originated from pathogens inside the cell.
Certain cells of the immune system may also encounter antigens that are not inside body cells. These particles are typically phagocytized, digested, and then antigen fragments are attached to class II MHC proteins which are then moved to the surface. Antigens attached to class II MHC proteins communicate that the cell is not infected. It enables the cell to display the antigen to other cells so that they can become activated.
The cell in the drawing below is not infected. The presence of antigen fragments attached to class II MHC proteins indicates that the antigens originated outside of the cell.
In summary, antigens attached to class I MHC proteins indicate that the cell displaying the antigen is infected; the antigen originated inside the cell. Antigens attached to class II MHC proteins indicate that the cell is not infected because the antigen originated outside of the cell; it was phagocytized.
Summary Diagram of Adaptive Immunity
Cell-mediated Immunity and T lymphocytes
Cell mediated immunity involves the use of T lymphocytes (T cells) to fight other body cells that may have become infected or changed such as virus-infected cells and cancer cells. It also fights single-celled fungi and other parasites, and the cells of an organ transplant.
All lymphocytes are produced in the bone marrow. T lymphocytes move to the thymus to mature. B lymphocytes mature in the bone marrow.
T cells must become activated before they function in immunity. Activated helper T cells are needed to activate cytotoxic T cells, which are used to destroy infected cells and some cancer cells. Activated helper T cells are also needed to activate B lymphocytes needed in antibody-mediated immunity.
T cells contain antigen receptors (T-cell receptors) on their surface and the cells become activated when the antigen receptors bind with antigen/MHC complexes from a host cell. There are millions of different kinds of antigen receptors on the surface of T cells but all of the receptors on the surface of a single T cell are identical; they are all capable of binding with the same antigen/MHC complex. Other T cells have different antigen receptors.
The type of antigen receptor is due to genetics. When a T cell is initially activated, it divides by mitosis to produce a clone of cells, each with identical antigen receptors. T cells with antigen receptors that do not match the antigen will not bind with the antigen and will not be activated or cloned.
T cells that do not recognize body cells (MHC) are eliminated in the thymus before they mature. This process, called thymic selection is necessary to prevent T cells from destroying normal, healthy body cells. Thymic selection involves both positive and negative selection as described below.
T cells that are unable to bind to MHC molecules in the thymus undergo apoptosis. Cells that do recognize MHC molecules do not die. Positive selection therefore enables the proliferation of T cells that are able to recognize self MHC markers.
Negative selection occurs when T cells that recognize “self” antigens undergo apoptosis.
Positive and negative thymic selection ensures that T cells recognize self MHC but not self antigens.
Helper T Cells
Helper T cells cannot recognize antigens unless an antigen-presenting cell such as a dendritic cell or a macrophage presents an antigen to them.
The antigen-presenting cell first phagocytizes the antigen (or bacterium, virus, etc.), digests the particles, and moves fragments of the foreign antigens to its surface linked to class II MHC proteins.
Activated helper T cells are produced when the antigen receptors of a T cell attach to antigens displayed on type II MHC proteins of antigen-displaying cells. After activation, they divide to produce a clone of identical helper T cells. These new activated helper T cells are able to activate other T cells and B cells by secreting cytokines.
This process is summarized below:
- CD4+ T cell encounters an antigen presenting cell with antigen-MHC type II → clone of T cells → some become active helper T cells (effector cells), others become memory helper T cells → activate B cells and cytotoxic T cells
HIV (the virus that causes AIDS) attacks helper T cells as well as other cells in the immune system. HIV therefore prevents adaptive immunity from becoming activated.
Cytotoxic T Cells
Infected cells contain antigens attached to type I MHC proteins on their surface. Cytotoxic T cells (also called killer T cells) kill these infected cells.
Cytotoxic T cells must first become activted before they can kill other cells. A clone of cytotoxic T cells is produced when a T cell interacts with a dendritic cell displaying antigen. The production of a clone also requires the presence of cytokines secreted by helper T cells (discussed earlier). Some of the cloned cells are cytotoxic T cells (effector cells), others are memory cytotoxic T cells.
Cytotoxic T cells with receptors that recognize the antigen and also the MHC type 1 proteins of another cell will release proteins that kill the other cell, thus stopping the spread of infection. Some of the proteins released by cytotoxic T cells penetrate the target cell membrane, producing holes in the membrane. Salts and fluid enter through the holes, causing the cell to rupture. Other proteins released by the cytotoxic T cell enter the target cell and stimulate apoptosis.
This process is summarized below:
- CD8+ T cell interacts with an antigen-presenting cell displaying antigen in the presence of cytokines from helper T cells → clone of T cells → some become cytotoxic T cells, othters become memory cytotoxic T cells → cytotoxic T cells kill infected cells (cells with with antigen-MHC type I)
Some cancer cells display abnormal antigens in type I MHC proteins and are killed by cytotoxic T cells.
Some of the cloned helper T cells become memory helper T cells and some of the cloned cytotoxic T cells become memory cytotoxic T cells. These memory cells persist after the infection and are available for activation if the body encounters the same infection in the future.
Antibody-mediated (Humoral) Immunity
Antibodies (immunoglobins) are similar to antigen receptors except that they are not attached to cells. They are Y-shaped molecules with a constant region and two binding sites that vary from one antibody to the next.
Particles that are bound to antibodies are foreign because, like antigen receptors, the body does not normally produce antibodies that are able to bind to its own antigens.
The following occur to foreign cells, particles, or molecules that have entered the body:
- Opsonization is the attachment of antibodies and compliment proteins to the surface. The presence of antibodies bound to antigens enhances phagocytosis.
- Neutralization- Toxic molecules that are attached to antibodies may not be able to affect cells.
- Agglutination- Bacteria, viruses, and other particles may agglutinate (clump together) because each antibody is capable of binding to two antigens. If the antigens are chemicals that are dissolved in the body fluids, the clumps of antibody-bound particles will precipitate. Antigens attached to cells will cause the cells to clump together and the clumps are then phagocytized. Agglutination of pathogens can stop the spread of the infection.
- Activation of the complement system- Membrane attack complexes form and produce holes in the plasma membranes of bacterial cells, killing the cell.
- Antibody-dependent Cell-mediated Cytotoxicity enables the destruction of large cells or organisms such as parasitic worms. Antibodies attached to these types of targets cause their destruction by secetions from eosinophils, macrophages, and natural killer cells.
During our life, we will encounter over 1 million different antigens, so we need at least 1 million different antibodies, each corresponding to a specific antigen. It has been estimated that our bodies are able to produce 100 million different kinds of antibodies.
Antibodies are produced by a special kind of B lymphocyte called plasma cells
Classes of Antibodies
There are 5 different classes of antibodies (IgA, IgD, IgG, IgH, IgM).
IgG comprise approximately 80% of the antibodies in blood serum. They are Y-shaped with two binding sites. They are able to leave the blood vessels and enter tissue fluids. They can also cross the placenta. They protect against bacteria, viruses, and toxins. They are able to activate the compliment system and enhance phagocytosis of cells and particles with bound antibody.
IgM antibodies look like five IgG antibodies attached in a ring by their stem area forming a pentamer. Due to their large number of binding sites (10), they are effective in attaching to multiple particles, forming a clump. This class of antibody is short-lived, making it useful for diagnosing disease.
IgA are the most common form in the mucous membranes and secretions (mucus, tears, saliva, milk). They are usually a monomer in serum but a dimer in secretions. Their main function appears to be prevent attachment of microbes to mucosal surfaces.
IgD are Y-shaped. They are found on the surface of B-cells.
IgE are Y-shaped. The stem region binds to receptors on mast cells and basophils. These cells release histamine when bound to antibodies that are bound to antigen.
Antibody Structure and Diversity
An antibody is composed of two identical light chains of amino acids and two identical heavy chains arranged in the shape of a "Y". Each antibody contains a constant region that does not vary from antibody to antibody and it also contains a variable region that does vary. The antigen binding site is within the variable region. The structure shown below is typical of IgM antibodies and of antigen receptors on B cells. The antigen receptors of T cells have only one antigen binding site.
The human genome contains approximately 20,000 genes but humans have approximately 100,000,000 different antibodies and antigen receptors. This large number of antibodies and receptors is possible due to rearrangements of randomly-selected regions of DNA when lymphocytes mature.
For example, an immature B lymphocyte contains a large region of DNA that will become the functional gene. When the lymphocyte matures, randomly selected regions from two different areas of this DNA will be reassembled to form the part of the gene that codes for the variable region of the antibody. The two regions are called the V region (red in the diagram below) and the J region (green). The DNA between the V and the J areas is deleted. The two randomly selected regions are combined with a constant region (C region) to form the functional gene. DNA between the randomly selected J area and the C area forms an intron. Its genetic code is deleted during the formation of a mature mRNA transcript.
The diagram below shows DNA from a lymphocyte before it is modified. A randomly-selected portion of the V region (orange) is combined with a randomly-selected portion of the J region (black). The DNA between these two regions is discarded.
The modified DNA is shown below. The remainder of the J region is an intron (green). It is removed from the pre-mRNA transcript.
The region of V that is in front of the randomly selected segment (red) is not transcribed. The DNA between V and J was eliminated. The region between C and the randomly-selected part of J is removed from the pre-mRNA transcript as an intron. The mRNA transcript is shown below.
Because the DNA of the lymphocyte is changed, all of the antibodies produced by the cell will be identical. Moreover, when the cell reproduces by mitosis, all of its descendents will be genetically identical and produce the same kind of antibodies.
The variable region of the light and the heavy chains of antibodies and of B-cell and T-cell receptors are created by a similar process to that described above.
B lymphocytes (B cells) mature in the bone marrow.
B cells have antigen receptors attached to their surface. They function to detect antigens by binding to the antigen.
The antigen receptors on the surface of B cells are mostly IgM and IgD.
All of the antigen receptors on the surface of one B cell are identical. A single B cell can therefore detect only one kind of antigen. Other B cells can detect other antigens. Our bodies have millions of different antigen receptors on B cells and can therefore detect millions of different antigens.
B cells must be activated before they can synthesize antibodies. Activation requires that the B cell attach to the antigen. The B cell must also be stimulated by a helper T cell that has also been exposed to the same antigen.
Once activated, the B cells will divide many times producing plasma cells, which in turn produce antibodies. The antibodies match the same epitope as the receptors on the surface of the B cell that was initially stimulated by epitope. The antibodies therefore can adhere to the type of invader that initially activated the B cell.
Plasma cells are capable of making different classes of antibody, all with the same antigenic specificity.
Plasma cells do not have antigen receptors on their surface and they live for approximately 4 to 5 days.
Clonal selection refers to the idea that activated B cells and T cells produce a clone of cells, each capable of responding to the same antigen that was responsible for activating the parent cell.
Large numbers of B-cells are found in the lymph nodes and in the spleen.
Pathogens typically have many different antigens on their surface. A single infection will therefore result in the production of many different kinds of antibodies, each capable of attaching to a specific antigen on the surface of the pathogen.
B cells that contain antigen receptors for the body's own tissues are eliminated before they reach maturity by a process called clonal deletion. This process is necessary to protect the body's cells from attack by the immune system. Clonal deletion of B cells occurs in the bone marrow.
Activation of B Cells
B cells must be activated before they divide to produce plasma cells (effector cells) and memory cells.
First, a specific antigen must attach to the antigen receptor on the surface of the B cell.
The particles bound to the antigen receptors of a B cell are brought into the cell by receptor-mediated endocytosis. This process encloses the particles within a vesicle and brings them into the cell. The vesicle will then fuse with a lysosome and digestive enzymes from the lysosome will digest the contents. The foreign proteins are broken down to peptide fragments.
The peptide fragments are attached to class II MHC proteins and then moved to the surface of the B cell.
A helper T cell that has been activated by exposure to the same antigen from an antigen displaying cell will bind to the B cell containing the antigen-MHC complex. The helper T cell will release signaling molecules called cytokines that stimulate the B cell to begin dividing and producing plasma cells and memory B cells.
This process is summarized below:
- a B cell phagocytizes antigen, attaches fragments to MHC type II proteins, moves the antigen-MHC complexes to the surface → an activated helper T cell with matching antigen receptors attaches and releases cytokines → the B cell divides by mitosis producing a clone of genetically identical cells → some of the clone become plasma cells which secrete antibody, others become memory B cells
Activated B cells also divide to produce more B cells with the same type of antigen receptors. They are called memory B cells because they may remain in the body for many years, ready to respond to the same antigen. Memory helper T cells are also long-lived, enabling a quick response to the same infection.
Primary and Secondary Immune Response
There is a time delay from the time of first exposure to an antigen to the time when significant amounts of antibodies are produced. This is because B cells and T cells must be stimulated as discussed above. After this, clonal selection produces plasma cells and plasma cells produce antibodies. This sequence of events is called the primary immune response. Peak antibody production occurs between 10 and 17 days after initial exposure to the antigen.
After a primary immune response has occurred, memory B cells and memory T cells remain in the body. Future exposure to the same antigen will result in antibody production sooner and at higher levels due to the presence of these memory cells. This response to a subsequent infection is a secondary immune response.
Active and Passive Immunity
Active immunity is produced in individuals by administering foreign antigens. These antigens may come from weakened or dead microorganisms. This process is called vaccination.
Genetically engineered bacteria are currently being used to produce some antigens. Examples: malaria, hepatitis B.
After exposure to antigens in a vaccine, the level of antibodies in the blood begins to increase after several days, levels off, then declines. After a secondary exposure (called a booster), the level increases rapidly.
Memory B cells and memory T cells allow an individual to be actively immune. If the individual is exposed to the disease, a rapid immune response will occur because they already have large numbers of the correct B and T cells.
Passive immunity occurs when an individual receives antibodies instead of making their own. Passive immunity is short-lived because the person's B and T cells have not been stimulated to produce antibodies. The immunity lasts only as long as the antibodies they received remain in their bloodstream.
Examples of Passive Immunity
Newborn babies have antibodies they received from their mother.
Breast-fed babies receive antibodies from their mother's milk.
Allergies are due to an overactive immune system.
Allergens are antigens that stimulate B cells to release IgE antibodies. IgE antibodies attach to mast cells in the connective tissues and to basophils in the blood. IgE antibodies attached to mast cells and basophils are able to bind to antigens. Mast cells and basophils will release histamine if their IgE antibodies attach to antigens (allergens).
Histamine causes mucus secretion, airway constriction, and inflammation due to blood vessels leaking. Leaky blood vessels cause the tissues to swell.
Allergy shots stimulate the body to produce high levels of antibodies. The antibodies react with the allergens before they have a chance to interact with the mast cells.
Functions of the Lymphatic System
1. take up excess tissue fluid and return it to the circulatory system
2. absorb fats at the intestinal villi and transports it to the circulatory system
3. defend against disease
Lymphatic vessels are similar to veins, including the presence of valves. They depend on the movement of skeletal muscles to move the fluid inside.
The fluid they contain is called lymph.
They empty into the circulatory system via the thoracic duct and the right lymphatic duct. The thoracic duct is much larger than the right lymphatic duct.
Lymph nodes are small (1-25 mm), spherical or ovoid structures that are connected to lymphatic vessels. They contain open spaces (sinuses), each with many leukocytes which function to remove infectious pathogens and foreign particles.
The structures listed below are groups of nodules that also function to purify lymph:
- tonsils - back of mouth
- adenoids - back of mouth above the soft palate
The spleen stores blood.
The spleen contains populations of lymphocytes and macrophages. As blood passes through the spleen, it is purified in much the same way that lymph is purified as it passes through the lymph nodes; bacteria and worn-out or damaged red blood cells are removed.
T lymphocytes mature in the thymus.
Microfold cells (M cells) on Peyer's patches and other lymphoid tissue in the intestinal wall act as a "surveillance" system by phagocytizing samples of antigens and microorganisms in the intestine and moving the antigens across the epithelium to areas rich in lymphocytes, dentritic cells, and macrophages. These cells then move to a lymph node where they can induce an immune response to the antigens.
Most leukocytes are produced in the bone marrow. T lymphocytes mature in the thymus gland, small intestine, and in the skin.
Autoimmune diseases result when the body produces antibodies that are capable of binding to its own tissues. They often appear in individuals that have recovered from other infections. Somehow the body seems to have learned to recognize its own antigens.
Myasthenia gravis - neuromuscular junctions are weakened
Multiple sclerosis - the myelin sheath of nerve fibers is attacked
Lupus erythematosus - Lupus is a chronic inflammatory disease. The skin, joints, kidneys and blood are most often affected but other organs may be affected as well.
Rheumatoid arthritis - the membranes that surround the joints are attacked
Type I diabetes - the insulin-producing cells (beta cells) of the pancreas are attacked
Neutrophils - phagocytize pathogens and foreign particles
Macrophages - phagocytize pathogens and foreign particles; function as antigen-presenting cells that activate T cells
Dendritic cells - phagocytic cells located on body surfaces that are in contact with the external environment; function as antigen-presenting cells that activate T cells
Monocytes - move out of the blood into other tissues and become macrophages
Eosinophils - kill parasites that are too large to phagocytize
Mast cells - secrete histamine when IgE receptors bind to antigen
Basophils - secrete histamine when IgE receptors bind to antigen
Natural Killer cells - kill virus-infected cells and cancer cells
B-lymphocytes - when stimulated, divide by mitosis to produce the following cell types:
- Plasma cells - produce antibodies
- Memory B lymphocytes - long-lived cells that are available to become activated if the body is exposed to the same antigen in the future.
- Helper T cells - secrete cytokines which activates B cells and cytotoxic T cells
- Cytotoxic T cells - attack cells that bear antigens attached to MHC type 1 proteins
- Memory helper T lymphocytes and memory cytotoxic T lymphocytes - long-lived cells that are available to become activated if the body is exposed to the same antigen in the future.