Protecting Your Body

The internal environment of the human body provides attractive conditions for growth of bacteria, viruses, and other organisms. Although some of these organisms can live symbiotically within humans, many either cause destruction of cells or produce toxic chemicals. To protect against these foreign invaders, three lines of defense are employed: nonspecific barriers that deter the entrance of invaders and both nonspecific and specific defenses against invaders inside the body. A nonspecific defense is a rapid response to a wide range of pathogens. A specific defense, delivered by the immune system, takes several days to mount and targets specific invaders that escape the attack of the nonspecific defense.

Nonspecific Barriers

The skin and mucous membranes provide a nonspecific first line of defense against invaders entering through the skin or through openings into the body. The first line of defense features the following mechanisms:

Skin is a physical and hostile barrier covered with oily and acidic (pH from 3 to 5) secretions from sebaceous and sweat glands, respectively.

Antimicrobial proteins (such as lysozyme, which breaks down the cell walls of bacteria) are contained in saliva, tears, and other secretions found on mucous membranes.

Cilia that line the lungs serve to sweep invaders out of the lungs.

Gastric juices of the stomach, by the action of hydrochloric acid or enzymes, kill most microbes.

Symbiotic bacteria found in the digestive tract and the vagina out-competes many other organisms that could cause damage.

Nonspecific Defenses

The second line of defense consists of mechanisms or agents that indiscriminately challenge foreign invaders that are inside the body.

Phagocytes are white blood cells (leukocytes) that engulf pathogens by phagocytosis. They include neutrophils, monocytes, and eosinophils. Monocytes enlarge into large phagocytic cells called macrophages.

Natural killer cells (NK cells) are lymphocytes (white blood cells that mature in lymphoid tissues). NK cells kill pathogen-infected body cells or abdominal body cells (such as tumors).

Complement is a group of about 20 proteins that “complement” defense reactions. These proteins help attract phagocytes to foreign cells and help destroy foreign cells by promoting cell lysis (breaking open the cell).

Interferons (IFNs) are substances secreted by cells invaded by viruses and that stimulate neighboring cells to produce proteins that help them defend against the viruses. Certain IFNs (such as gamma-IFN) also amplify the activity of macrophages and natural killer cells.

The inflammatory response is a series of nonspecific events that occur in response to pathogens. The response typically produces redness, swelling, heat, and pain in the target area and often the area is disabled. When skin is damaged, for example, and bacteria, other organisms, or toxic substances enter the body, the following events occur:

o A chemical alarm is generated in the injured area. Injured cells and nearby circulating cells release chemicals that initiate defensive actions and sound an alarm to other defense mechanisms. These chemicals include histamine (mostly secreted by basophils, white blood cells found in connective tissue), kinins, prostaglandins (PGs), and complement.

o Vasodilation (dilation of blood vessels), stimulated by histamine and other chemicals, increases blood supply to the damaged area. This causes redness and an increase in local temperature. The increase in temperature stimulates white blood cells and makes the environment inhospitable to pathogens.

o Vascular permeability increases in response to alarm chemicals. As a result, white blood cells, clotting factors, and body fluids move more quickly through blood vessel walls and into the injured area. The increase in body fluids that results causes local edema (swelling). Edema may produce pain if nearby nerve endings experience pressure. Pain may also occur when nerve endings are exposed to bacterial toxins, kinins, and prostaglandins. (Aspirin reduces pain by inhibiting the production of prostaglandins.)

o Phagocytes arrive at the site of injury and engulf pathogens and damaged cells. Phagocytes find the site of injury by chemotaxis, the movement of cells in response to chemical gradients (provided here by alarm chemicals).

o Complement helps phagocytes engulf foreign cells, stimulates basophils to release histamine, and helps lyse foreign cells.

Fever is a total body response to infection characterized by elevated body temperature. An elevated temperature increases cellular metabolism (accelerating

cellular repairs), amplifies the effect of alarm chemicals, and creates a hostile environment for bacteria. An excessively high fever may cause the breakdown of enzymes necessary for cellular metabolism, and death may result.

The Immune System

The immune system is the third line of defense. It consists of mechanisms and agents that target specific antigens (Ags). An antigen is any molecule, usually a protein or polysaccharide, that can be identified as foreign or nonself. It may be a toxin (injected into the blood by the sting of an insect, for example), a part of the protein coat of a virus, or a molecule unique to the plasma membranes of bacteria, protozoa, pollen, or other foreign cells. Once the antigen is recognized, an agent is released that targets the specific antigen. In the process of mounting a successful defense, the immune system accomplishes five tasks:

Recognition. The antigen or cell is recognized as nonself. To differentiate self from nonself, unique molecules on the plasma membrane of cells called the major histocompatibility complex (MHC) are used as a means of identification.

Lymphocyte selection. The primary defending cells of the immune system are certain white blood cells called lymphocytes. The immune system potentially possesses billions of lymphocytes, each equipped to target a different antigen. When an antigen, or nonself cell, binds to a lymphocyte, the lymphocyte proliferates, producing numerous daughter cells, all identical copies of the parent cell. This process is called clonal selection because the lymphocyte to which the antigen effectively binds is “selected” and subsequently reproduces to make clones, or identical copies, of itself.

Lymphocyte activation. The binding of an antigen or foreign cell to a lymphocyte may activate the lymphocyte and initiate proliferation. In most cases, however, a costimulator is required before proliferation begins. Costimulators may be chemicals or other cells.

Destruction of the foreign substance. Lymphocytes and antibodies destroy or immobilize the foreign substance. Nonspecific defense mechanisms (phagocytes, NK cells) help eliminate the invader.

Memorization. Long-lived “memory” lymphocytes are produced and can quickly recognize and respond to future exposures to the antigen or foreign cell.

Major Histocompatibility Complex

The major histocompatibility complex (MHC) (also called human leukocyte antigens, HLAs) is the mechanism by which the immune system is able to differentiate between self and nonself cells. The MHC is a collection of glycoproteins (proteins with a carbohydrate) that exist on the plasma membranes of nearly all body cells. The proteins of a single individual are unique, originating from 20 genes, with more than 50 variations per gene between individuals. Thus, it is extremely unlikely that two people, except for identical twins, will possess cells with the same set of MHC molecules.

The immune system is able to identify nonself cells by aberrations in the MHC displayed on the plasma membrane. There are two groups of MHC molecules, and each group generates different markings on the plasma membrane:

MHC-I glycoproteins are produced by all body cells (except red blood cells). When a cell becomes cancerous or is invaded by a virus, unfamiliar proteins are synthesized in the cell. These proteins are endogenous antigens—that is, antigens produced inside the cell. Portions of these antigens are combined with MHC-I glycoproteins and, when displayed on the plasma membrane, indicate a nonself cell.

MHC-II glycoproteins are produced only by antigen-presenting cells (APCs)—mostly macrophages and B cells. APCs actively ingest exogenous antigens, antigens that originate outside the cell. Exogenous antigens include viruses, toxins, pollen, or bacteria that are circulating in the blood, lymph, or body fluids. APCs break down the antigens and incorporate pieces of them with MHC-II proteins. This aberrant display of MHC markers is recognized as nonself.

Lymphocytes

The primary agents of the immune response are lymphocytes, white blood cells (leukocytes) that originate in the bone marrow (like all blood cells) but concentrate in lymphoid tissues such as the lymph nodes, the thymus gland, and the spleen. When lymphocytes mature, they become immunocompetent, or capable of binding with a specific antigen. An immunocompetent lymphocyte displays unique proteins on its plasma membrane that act as antigen receptors capable of binding to a specific antigen. Because all of the antigen receptors of an individual lymphocyte are identical, only a specific antigen can bind to an individual lymphocyte. The kind of antigen receptors displayed by a particular lymphocyte is determined by somatic recombination, a shuffling of gene segments during lymphocyte maturation. By mixing gene segments, more than one billion different antigen receptors can be generated.

Here are the various kinds of lymphocytes:

B cells (B lymphocytes) are lymphocytes that originate and mature in the bone marrow. The antigen receptors of B cells bind to freely circulating antigens. When B cells encounter antigens that bind to their antigen binding sites, the B cells proliferate, producing two kinds of daughter cells, plasma cells and memory cells.

o Plasma cells are daughter cells of B cells. Each plasma cell releases antibodies, proteins that have the same antigen binding capability as the antigen receptors of its parent B cell. Antibodies circulate through the body binding to the specific antigens that stimulated the proliferation of plasma cells.

o Memory B cells are long-lived daughter cells of B cells that, like plasma cells, produce antibodies. However, memory cells do not release their antibodies in response to the immediate antigen invasion. Instead, the

memory cells circulate in the body and respond quickly to eliminate any subsequent invasion by the same antigen. This mechanism provides immunity to many diseases after the first occurrence of the disease.

T cells (T lymphocytes) are lymphocytes that originate in the bone marrow, but mature in the thymus gland. The antigen receptors of T cells bind to self cells that display foreign antigens (with MHC proteins) on their plasma membrane. When T cells bind to these aberrant self cells, they divide and produce the following kinds of daughter cells:

o Cytotoxic T cells (killer T cells) are activated when they recognize antigens that are mixed with the MHC-I proteins of self cells. Following activation, cytotoxic cells proliferate and destroy the recognized cells by producing toxins that puncture them, thus causing them to lyse.

o Helper T cells are activated when they recognize antigens that are mixed with the MHC-II proteins of self cells. Proliferation produces helper T cells that intensify antibody production of B cells. Helper T cells also secrete hormones called cytokines that stimulate the proliferation of B cells and T cells.

o Suppressor T cells are believed to be involved in winding down a successful immune response and in preventing the attachment of uninfected self cells.

o Memory T cells are long-lived cells possessing the same antigen receptors as their parent T cell. Like memory B cells, they provide a rapid defense to any subsequent invasion by the same antigen.

Antibodies

Antibodies are proteins that bind to specific antigens. B cells, located in lymphoid tissue, release the antibodies, which then circulate in the blood plasma, lymph, or extracellular fluids. Some antibodies migrate to other areas of the body, such as the respiratory tract or the placenta, or enter various body secretions, such as saliva, sweat, and milk. Additional properties of antibodies include the following:

There are five classes of antibodies (or immunoglobulins): IgA, IgD, IgE, IgG, and IgM. Antibodies circulating in the blood are primarily IgG, IgA, and IgM, IgD and a second form of IgM antibodies are found on the plasma membranes of B cells where they act as antigen receptors. IgE antibodies attach to basophils and mast cells (both white blood cells found in connective tissue) and induce them to secrete histamine.

The basic structure of an antibody is Y-shaped protein that consists of constant and variable regions. The variable regions are sequences of amino acids that differ among antibodies and give them specificity to antigens.

Antibodies inactivate antigens by binding to them and forming an antigen-antibody complex. Inactivation is followed by macrophage phagocytosis or lysis brought about by complement proteins. Inactivation may also cause agglutination (clumping) of antigens or foreign cells.

Co-Stimulation

In some immune responses, a B cell or T cell becomes activated when an antigen or nonself cell binds to it. Activation then initiates proliferation. In most immune responses, however, activation requires the presence of a costimulator. That two signals, an antigen and a costimulator, are required to initiate the immune response ensures that healthy self cells are not destroyed. Costimulation may occur in two ways:

Cytokines, released by helper T cells and APCs, act as costimulators. Cytokines are protein hormones that influence cell growth. When a helper T cell becomes activated or an APC engulfs an antigen, the helper T cell or APC secretes a cytokine called interleukin.

Helper T cells and APCs act as costimulators. Activated T cells or APCs that display antigens activate B cells or T cells when they temporarily bind to them.

Humoral, Cell-Mediated Immune Responses

The immune system distinguishes two groups of foreign substances. One group consists of antigens that are freely circulating in the body. These include molecules, viruses, and foreign cells. A second group consists of self cells that display aberrant MHC proteins. Aberrant MHC proteins can originate from antigens that have been engulfed and broken down (exogenous antigens) or from virus-infected and tumor cells that are actively synthesizing foreign proteins (endogenous antigens). Depending upon the kind of foreign invasion, two different immune responses occur:

The humoral response (or antibody-mediated response) involves B cells that recognize antigens or pathogens that are circulating in the lymph or blood (“humor” is a medieval term for body fluid). The response follows this chain of events:

1. Antigens bind to B cells.

2. Interleukins or helper T cells costimulate B cells. In most cases, both an antigen and a costimulator are required to activate a B cell and initiate B cell proliferation.

3. B cells proliferate and produce plasma cells. The plasma cells bear antibodies with the identical antigen specificity as the antigen receptors of the activated B cells. The antibodies are released and circulate through the body, binding to antigens.

4. B cells produce memory cells. Memory cells provide future immunity.

The cell-mediated response involves mostly T cells and responds to any cell that displays aberrant MHC markers, including cells invaded by pathogens, tumor cells, or transplanted cells. The following chain of events describes this immune response:

1. Self cells or APCs displaying foreign antigens bind to T cells.

2. Interleukins (secreted by APCs or helper T cells) costimulate activation of T cells.

3. If MHC-I and endogenous antigens are displayed on the plasma membrane, T cells proliferate, producing cytotoxic T cells. Cytotoxic T cells destroy cells displaying the antigens.

4. If MHC-II and exogenous antigens are displayed on the plasma membrane, T cells proliferate, producing helper T cells. Helper T cells release interleukins (and other cytokines) which stimulate B cells to produce antibodies that bind to the antigens and stimulate nonspecific agents (NK and macrophages) to destroy the antigens.

Supplements to the Immune Response

Three important agents are used in medicine to supplement the immune response:

Antibiotics are chemicals derived from bacteria or fungi that are harmful to other microorganisms.

Vaccines are substances that stimulate the production of memory cells. Inactivated viruses or fragments of viruses, bacteria, or other microorganisms are used as vaccines. Once memory cells are formed, the introduction of the live microorganism will stimulate a swift response by the immune system before any disease can become established.

Passive immunity is obtained by transferring antibodies from an individual who previously had a disease to a newly infected individual. Newborn infants are protected by passive immunity through the transfer of antibodies across the placenta and by antibodies in breast milk.

ANATOMY &PHYSIOLOGY—LECTURE NOTES—IMMUNE RESPONSE

To repel all the bacteria, viruses, and fungi that make a daily attempt to invade and colonize, the body relies on the immune system.

Immunity is the ability to resist damage from foreign substances (microorganisms, harmful chemicals). Immunity is categorized as being innate or adaptive.

Innate immunity provides the basic means for the destruction of foreign organisms. It recognizes and destroys certain foreign substances, but the response to them is the same during each encounter. It consists of mechanical barriers as well as certain cells and chemical mediators. The main barriers are skin and mucosae. Cells and chemicals include granulocytes, monocytes, macrophages, antimicrobial proteins, etc. A characteristic response of the innate system is inflammation.

The adaptive immune system consists of cells that attack particular antigens in a particular way. It improves and enhances the efficiency of the innate mechanisms and remembers the infection the next time it is encountered. Specificity (the ability to distinguish pathogens) and memory (the ability to respond more rapidly to a previously encountered pathogen) are characteristics of adaptive immunity, but not of innate immunity.

Skin helps repel pathogens in many ways. It’s highly keratinized, which provides a physical barrier to pathogens. The acidity of sweat can kill some pathogens. Sebum is bactericidal.

Mucous membranes are another major barrier to pathogens. They line the digestive, respiratory, urinary, and reproductive tracts - all of which are potential entrance points for pathogens. They are often covered in sticky, pathogen-trapping mucus. Respiratory mucosa is also ciliated. Cilia sweep bacteria-laden mucus upward to the pharynx where it can be swallowed. Coughing and sneezing also assist in expulsion.

A variety of body fluids also provide innate defense. Tears, saliva, and urine wash away microorganisms. Saliva, intestinal fluid, and tears contain lysozyme, an enzyme that destroys bacteria. The acidity of certain mucosal secretions (gastric and vaginal) can impair pathogens.

Growth of disease-causing organisms is inhibited by the growth of non-pathogenic bacteria in the gastrointestinal and urogenital tracts. These bacteria successfully compete with the pathogenic ones for nutrients and resources.

WBCs and derivatives are the most important cellular component of the innate immune system. Recall that WBCs can exit blood vessels (diapedesis), converge upon areas of infection/damage (positive chemotaxis) and move over, btwn, and through other cells. Neutrophils are small phagocytic cells that are usually the first to enter infected tissues. They function primarily as bacteria killers. Macrophages are large phagocytic cells derived from monocytes. Macrophages may be free (able to move thru tissue spaces) such as the alveolar macrophages in the lungs or fixed (permanent residents of a particular organ) such as the microglia of the CNS. Macrophages perform phagocytosis whereby they ingest something (a bacterium, particulate matter, etc.) and enclose it within a membrane-bound vesicle. The process begins with the adherence of a microbe to the phagocyte. The probability of this occurring is increased when antibodies or complement proteins have already bound to the microbe (a process called opsonization). The phagocyte then extends membrane “arms” that wrap the microbe and engulf it, forming a membrane-bound vesicle containing the pathogen. This vesicle is known as a phagosome. The phagosome then will fuse with a lysosome, an organelle that contains digestive enzymes. The enzymes will then destroy the engulfed material. Whatever indigestible material remains is then exocytosed.

Natural killer cells are another innate cellular defense. They’re a specialized type of lymphocyte that attacks and destroys virus-infected cells and cancer cells.

Innate defense is also provided by a variety of antimicrobial proteins. One class is the interferons. There are several types of interferons. We’ll discuss one particular brand. These interferons are proteins produced by cells that have been infected with a virus. The interferons then diffuse to nearby cells and stimulate them to synthesize a protein that prevents viral replication. This prevents copies of the original virus from taking over neighboring cells. Interferons thus do not save the infected cell but prevent nearby cells from being infected. The same interferons can act against many different types of viruses.

Complement refers to a group of about 20 plasma proteins synthesized by the liver.

They’re normally found in the blood in an inactive state. They may be activated by interacting directly with a pathogen or by members of the adaptive immune system. Activation of complement results in 4 things:

Chemotaxis – activated complement proteins attract WBCs.

Opsonization → binding of activated complement proteins to bacteria increases the likelihood of their phagocytosis.

Inflammation → activated complement proteins bind to basophils and mast cells and stimulate histamine release. This results in vasodilation and increased capillary permeability and inflammation.

Lysis → activated complement proteins can form a “membrane attack complex,” which is a tube that pierces the bacterial cell membrane. This allows salt and water to flow in and results in cell lysis.

The inflammatory response occurs whenever tissues are damaged. It helps to prevent pathogen spread, disposes of pathogens and debris, and sets the stage for repair. The signs of inflammation include heat, redness, swelling, pain, and loss of function. It begins when damaged tissues release inflammatory chemicals (histamine, prostaglandins, leukotrienes, kinins, etc.). These chemicals act to: increase WBC count, increase local capillary permeability, cause local vasodilation, attract WBCs to the injury site, and stimulate pain-sensitive neurons. The increase in vasodilation and capillary permeability yields an increase in blood flow and capillary fluid loss. This results in swelling, heat, redness, and increased access to the injury site by WBCs, complement proteins, antibodies, and clotting proteins.

Fever is a systemic response to infection associated with an abnormally high body temperature. Many WBCs and macrophages release chemicals called pyrogens in response to pathogen exposure. Pyrogens act on the body’s hypothalamic thermostat to raise body temperature. A mild increase in temperature can accelerate WBC function; impair bacterial metabolism; and cause the liver and spleen to sequester zinc and iron, two minerals necessary for bacterial survival. A major increase in body temperature can result in severe protein denaturation and possible loss of life.

The adaptive immune system responds in strong ways tailored to particular antigens. It differs from the innate system in that it’s specific, systemic, and improves its efficiency each time it encounters the same pathogen.

Antigens are substances that can provoke the adaptive immune system and cause a response. Most are large, complex molecules not normally found in the body. Thus they are non-self or foreign antigens. Haptens are small, foreign molecules that do not generate an immune response unless they are attached to a normal body protein. Self antigens are molecules produced by the body that stimulate the adaptive immune system. They can result in autoimmune disease.

The principal cells of adaptive immunity are the lymphocytes. There exist 2 main types of lymphocytes: B lymphocytes and T lymphocytes. Both are formed initially in the red bone marrow. B lymphocytes gain immunocompetence (i.e., mature) in the bone marrow while T lymphocytes gain immunocompetence in the thymus.

Immunocompetent B and T cells are composed of small groups of identical lymphocytes called clones. Each clone has many copies (104-106) of a receptor on its cell surface. The presence of one specific type of receptor allows each clone to bind/recognize and interact with 1 specific type of antigen. There are more than a million different varieties of clones, giving the lymphocytes a large variety of antigens to which they can respond. Once a B or T cell has become immunocompetent, the naïve cells will travel to the lymph nodes, spleen, or other lymphoid organs to await antigens.

Another cell type that plays a critical role in adaptive immunity is the antigenpresenting cell. The main APCs are the dendritic cells in connective tissue, and the macrophages.

They function by engulfing antigens and then presenting antigen fragments on their surface as a signal to Helper T cells (a type of T lymphocyte). They are basically identifying the invading antigens and then displaying it the specific appropriate lymphocyte and saying – “Hey these guys invaded us. Find them, build an army, and kill ‘em!”

There are 2 main components to the adaptive response: antibody-mediated immunity and cell-mediated immunity. The antibody-mediated response (a.k.a. the humoral response) is the body’s response to extracellular antigens, i.e., those antigens found within plasma, ISF, or lymph. Cell-mediated immunity refers to how the body deals with microorganisms that have invaded cells (e.g., viruses, certain bacteria and fungi). Bear in mind that these 2 branches will overlap and work together.

Let’s suppose a pathogen has invaded the body and is somewhere in the extracellular space (i.e., plasma, lymph, tissue fluid, etc). The 1st step in the body’s response is for an APC (i.e., a macrophage or dendritic cell) to engulf it. Once engulfed, the pathogen will be destroyed. Then resulting pieces (which we can consider antigens) will be displayed on the surface of the APC by a molecule known as a class II MHC protein. The antigen will be recognized by and stimulate a Helper T cell that contains the specific receptor matching the particular antigen. The Helper T cell must also receive a confirmation signal from the APC before it proceeds. This confirmation signal is called costimulation. The Helper T cell will now proliferate to form many more Helper T cells, which also respond to the same original antigen. These Helper T cells can release cytokines (which are chemicals that will stimulate the body’s innate defenses). The Helper T cells will also help activate B cells and/or Killer T cells.

Now let’s suppose that the same pathogen runs into a B cell that carries the specific receptor for it. The B cell will then engulf it, kill it, and display antigenic fragments on its own MHC II proteins. Once the antigen has been displayed to the previously mentioned Helper T cells, those Helper T cells will stimulate the B cell to begin dividing. Most of the resulting cells will be plasma cells. Plasma cells secrete up to 2000 antibodies per second. Each antibody will specifically bind to the original antigen and mark it for destruction. A small percentage of the clones will be memory cells. These memory cells have the ability to mount an almost immediate humoral response if the same antigen appears again in the future. NB: this entire process is referred to as clonal selection.

Antibodies are also called immunoglobulins, gamma globulins, or Ig’s. Each consists of 4 polypeptide chains that combine to form a Y-shaped structure known as an antibody

monomer. Each antibody monomer has 2 variable regions (the ends of the 2 arms of the Y) and a constant region (the stem of the Y). The variable regions contain the antigen binding sites. All antibodies released from the same plasma cell will have the same antigen-binding sites. Thus they will all be specific for the same antigen. The constant region binds to other immune chemicals or cells and determines the mechanism by which the bound antigen will be destroyed. The constant regions also determine the antibody class. There are 5 antibody classes: IgM, IgA, IgD, IgG, and IgE. Antibodies of each class have different constant regions and different roles and locations in the body.

Antibodies have 4 main mechanisms of action: precipitation, lysis, agglutination, and neutralization. Precipitation occurs when antibodies bind soluble antigens into clumps. This increases the likelihood of phagocytosis. Lysis occurs when antibodies activate complement. This results in the formation of a membrane attack complex, and bursting of the bacterial cell. Agglutination occurs when antibodies bind cell-bound antigens into clumps. This increases the likelihood of phagocytosis. Neutralization occurs when antibodies bind to and mask the dangerous portions of antigens, toxins, and viruses. Now let’s suppose that the original pathogen has begun invading the body cells. Antibodies are only effective against extracellular antigens. They’re useless against pathogens that have slipped inside body cells. This is where cell-mediated immunity comes into play. Fragments of intracellular proteins are displayed on the surface of every nucleated body cell by molecules known as class I MHC proteins. This gives a “window” into a cell, that T lymphocytes can “look in” to see if everything is ok. The combination of our original antigen and the MHC I protein displaying it will bind to and stimulate a Killer T cell that contains the specific receptor matching the original antigen. With a little stimulation from our aforementioned Helper T cells, the activated Killer T cell will begin to divide. This results in both mature killer T cells and memory killer T cells. Memory killer T cells will persist in case of a subsequent infection by the same pathogen. Mature killer T cells will set about to kill those body cells displaying the same specific antigen as the original one that began the activation process, e.g., cells infected by the same type of virus. Killer T cells release lethal chemicals that are capable of causing cell death.

It should be noted that Helper T cells are sometimes referred to as CD4 cells, while Killer T cells are sometimes referred to as CD8 cells.

Suppressor T cells are another class of T lymphocytes. They release cytokines that suppress the activity of B cells and certain T cells. This helps prevent runaway or unnecessary immune activity.

Let’s take a look at another aspect of antibody-mediated immunity. The initial encounter with a particular antigen is termed the primary immune response. It typically has a lag period of 3-6d btwn the time of exposure to the antigen and the appearance of antibodies specific for that antigen in the plasma. During this lag period clonal selection and antibody production both take place. Plasma antibody levels peak at about 10d and then decline. B/c the primary immune response results in memory cell production, it will differ from future responses. In the secondary response, the presence of memory cells primed for the original antigen will result in:

1) A shorter lag time.2) Plasma cells that remains alive and functioning for a much longer time.3) Achievement of higher antibody levels in a shorter time.4) Higher efficiency of binding between antibodies and antigens.

A similar form of immunological memory will occur with T cells.

Immunity can be achieved into basic ways. Active immunity is the result of memory cell production by the body in response to a foreign antigen. Passive immunity occurs when antibodies from another person (or animal) are transferred to a non-immune individual. Active immunity can be naturally adaptive in response to infection. It can also be artificially adaptive due to vaccination – the injection of dead or weakened pathogens into the body. This results in memory cell production, but spares the body of symptoms. Active immunity lasts for as long as the memory cells remain alive in the body. Truly long lasting immunity may require continual exposure to the pathogen. Passive immunity, since it does not involve memory cell production, has a much shorter duration than does active immunity – lasting only as long as the antibodies remain in the circulation. Passive immunity can be natural when antibodies cross the placenta and travel from the maternal bloodstream to the fetal bloodstream, or when antibodies are excreted in breast milk. It can be artificial when antibodies are given by injection.

Another class of lymphocytes are the Regulatory T Lymphocytes. They function to rein in the responses of B and T cells and make sure they do not go overboard.