Anatomy: Ch. 21 pt. 2 The Immune System
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Created by:
Jeannine_Torres on January 31, 2012
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173 terms
Terms | Definitions |
|---|---|
 lymphatic tissues | The WHAT are composed of a variety of lymphocytes and other cells with various roles in defense and immunity: NK cels, T cells, B cells, Macrophages, and dendritic cells |
| natural killer cells | WHAT are large lymphocytes that attack and destroy bacteria, transplanted tissue cells, and host cells (cells of one's own body) that have either become infected with viruses or turned cancerous. They are responsible for a mode of defense called immune surveillance. |
| T lymphocytes | (T cells) WHAT are lymphocytes that mature in the thymus and later depend on thymic hormones; the T stands for thymus-dependent. |
| B lymphocytes | (B cells) WHAT are lymphocytes that differentiate into plasma cells- connective tissue cells that secrete the antibodies of the immune system. They are named for an organ in chickens (the bursa) in which they were first discovered. However, you may find it more helpful to think of B for bone marrow, the site where the cells mature in humans. |
| macrophages | WHAT are very large, avidly phagocytotic cells of the connective tissues. They develop from monocytes that have emigrated from the bloodstream. They phagocytize tissue debris, dead neutrophils, bacteria, and other foreign matter. They alert the immune system to the presence of an enemy. Macrophages and other cells that do this are collectively called antigen-presenting cells (APCs). |
| dendritic cells | WHAT are branched, mobile APCs found in the epidermis, mucous membranes, and lymphatic organs. They play an important role in alerting the immune system to pathogens that have breached the body surfaces. They engulf foreign matter by receptor-mediated endocytosis rather than phagocytosis, but otherwise function like macrophages. |
| reticular cells | WHAT are branched stationary cells that contribute to the stroma of the lymphatic organs and act as APCs in the thymus. |
| first line of defense | WHAT consists of external barriers, notably the skin and mucous membranes, which are impenetrable to most of the pathogens that daily assault us. |
| second line of defense | WHAT consists of several nonspecific defense mechanisms against pathogens that break through the skin or mucous membranes. These defenses include leukocytes and macrophages, antimicrobial proteins, immune surveillance, inflammation, and fever. They work even against pathogens to which the body has never before been exposed. |
| third line of defense | WHAT is the immune system, which not only defeats a pathogen but leaves the body with a "memory" of it, enabling us to defeat it so quickly in future encounters that the pathogen causes no illness. (cellular and humoral immunity) |
| nonspecific resistance | The first two defenses are called WHAT because they guard equally against a broad range of pathogens and their effectiveness does not depend on prior exposure |
| specific defense | Immunity is called a WHAT because it results from prior exposure to a pathogen and usually provides future protection only against that particular one. |
| keratin | The skin surface is composed mainly of WHAT, a tough protein that few pathogens can penetrate. Furthermore, the surface is hostile to microbial reproduction. It is too dry and poor in nutrients to support much microbial growth. The skin is also coated with antimicrobial chemicals such as defensins and lactic acid. |
| defensins | WHAT are peptides that kill microbes by creating holes in their membranes |
| lactic acid | The skin is also coated with a thin film of WHAT (acid mantle) from sweat, which inhibits bacterial growth. |
| mucous membranes | The digestive, respiratory, urinary, and reproductive tracts are open to the exterior, making them vulnerable to invasion, but they are protected by WHAT? |
| mucus | WHAT physically ensnares microbes. Organisms trapped in the respiratory mucus are moved by cilia to the pharynx, swallowed, and destroyed by stomach acid. Microbes also are flushed from the upper digestive tract by saliva and from the lower urinary tract by urine |
| lysozyme | Mucus, tears, and saliva also contain WHAT, an enzyme that destroys bacteria by dissolving their cell walls. |
| hyaluronic acid | Beneath the epithelia of the skin and mucous membranes, there is a layer of areolar tissue. The ground substance of this tissue contains a giant glycosaminoglycan called WHAT, which gives it a viscous consistency. It is normally difficult for microbes to migrate through this sticky tissue gel. |
| hyaluronidase | Hyaluronic acid is normally difficult for microbes to migrate through this sticky tissue gel. Some organisms overcome this obstacle, however, by producing an enzyme called WHAT, which breaks it down to a thinner consistency that is more easily penetrated. Use of arthropod vectors (ticks, mosquitoes, fleas, lice, mosquitoes, etc.) to penetrate the skin. |
| phagocytes | If microbes get past the physical barrier of the skin and mucous membranes, they are attacked by WHAT that have a voracious appetite for foreign matter. Leukocytes and macrophages play especially important roles in both nonspecific defense and specific immunity and in both the second and third line of defense. |
| neutrophils | WHAT spend most of their lives wandering in the connective tissues killing bacteria. Phagocytize bacteria, release antimicrobial chemical. (antibacterial) |
| eosinophils | WHAT are found especially in the mucous membranes, standing guard against parasites, allergens (allergy-causing antigens), and other pathogens. They become especially concentrated at sites of allergy, inflammation, or parasitic infection. they help kill parasites such as tapeworms and roundworms by producing superoxide, hydrogen peroxide, and various toxic proteins including a neurotoxin. (antiparasitic, roles in allergy and inflammation) |
| basophils | WHAT secrete chemicals that aid the mobillity and action of other leukocytes: leukotrienes that activate and attract neutrophils and eosinophils; the vasodilator histamine, which increases blood flow and speeds the delivery of leukocytes to the area; and the anticoagulant heparin, which inhibits the formation of blood clots that would impede leukocyte motility. These substances are also produced by mast cells. (secrete histamine and herapin) |
| lymphocytes | WHAT are three basic categories: NK cells, T cells, and B cells. Immune surveillance, specific immunity. |
| monocytes | WHAT are leukocytes that emigrate from the blood into the connective tissues and transform into macrophages. Macrophages are widely distributed in the loose connective tissues. (Phagocytosis, antigen presentation- "present" antigens to activate other cells of immune system) |
| interferons | When certain cells are infected with viruses, they secrete proteins called WHAT? Like its "dying words" that alert neighboring cells and protect them from becoming infected. Interferons bind to surface receptors on those cells and activate second-messenger systems within. The alerted cell then synthesizes various proteins that defend it from infection. WHAT also activate NK cells and macrophages, which destroy infected cells before they can liberate a swarm of newly replicated viruses. WHAT confer resistance not only to viruses but also to cancer. |
| interferons | WHAT are secreted by WBC and other cells invaded by viruses, alert neighboring cells to defend themselves in advance, activate NK cells and macrophages |
| complement system | WHAT is a group of 30 or more globulins that make powerful contributions to both nonspecific resistance and specific immunity. It "completes the action of antibody" and indeed is the principal means of pathogen destruction in antibody-mediated immunity. |
| liver | Complement proteins are synthesized mainly by the WHAT. They circulate in the blood in inactive form and are activated in the presence of pathogens. In their inactive form, the proteins are named with the letter C and a number such as C3. Activation splits them into fragments (C3a and C3b) |
| four | Activated complement brings about HOW MANY methods of pathogen destruction: inflammation, immune clearance, phagocytosis, and cytolysis |
| three | There are HOW MANY routes: the classical, alternative, and lectin pathways. |
| classical pathway | WHAT pathway requires an antibody molecule to get started. Antigen-antibody complex form on pathogen surface. Reaction cascade (complement fixation) |
| alternative and lectin | The WHAT and WHAT pathways require no antibodies and thus belong to our nonspecific defenses. |
| alternative pathway | The WHAT pathway is C3 dissociates into fragment C3a and C3b. C3b binds to pathogen surface. Reaction cascade and autocatalytic effect. Then C3 dissociates into C3a and C3b. |
| lectin pathway | The WHAT pathway are plasma proteins that bind to carbohydrates. Then proceeds with reaction cascade and then C3 splits into C3a and C3b |
| inflammation | C3a stimulates mast cells and basophils to secrete histamine and other inflammatory chemicals. It also activates and attracts neutrophils and macrophages. (Isolates and destroys pathogens, removed tissue debris, begins tissue repair) |
| immune clearance | Ag-Ab complexes to red blood cells. As these RBCs circulate through the liver and spleen, the macrophages of those organs strip off and destroy the Ag-Ab complexes, leaving the RBCs unharmed. (Ag-Ab complexes bind to RBCs; macrophages of liver and spleen strip them off and dispose of them) |
| phagocytosis | Bacteria, viruses, and other pathogens are phagocytized and digested by neutrophils and macrophages. However, these phagocytes cannot easily internalize "naked" microorganisms. |
| opsonization | C3b assists the "naked" organisms from phagocytosis by the process of WHAT? It coats microbial cells and serves as binding sites for phagocyte attachment. WHAT "butters up" the foreign cells to make them more appetizing. |
| cytolysis | WHAT by membrane attack complex (MAC). MAC forms hold in target cell membrane, rupturing target cell. |
| immune surveillance | WHAT is a phenomenon in which natural killer (NK) cells continually patrol the body "on the lookout" for pathogens or diseased host cells. They attack and destroy bacteria, cells of transplanted organs and tissues, cells infected with viruses, and cancer cells. |
| perforins | Upon recognition of an enemy cell, the NK cell binds to it and releases proteins called WHAT, which polymerize in a ring and create a hole in its plasma membrane. The hole allows a rapid flow of water and salts into the enemy cell, which may kill it but is not very effective alone. |
| granzymes | The NK cell also secretes a group of protein-degrading enzymes called WHAT? which enter the pore made by the perforins. Inside the enemy cell, the granzymes destroy cellular enzymes and induce apoptosis (programmed cell death) |
| inflammation | WHAT is a local defensive response to tissue injury of any kind, including trauma and infection |
| inflammation | WHATS purpose is to 1. limit the spread of pathogens and ultimately destroy them 2. remove the debris of damaged tissue 3. initiate tissue repair. It is characterized by four cardinal signs: redness, swelling, heat and pain |
| itis | Words ending in the suffix -WHAT denote inflammation of specific organs and tissues: arthritis, encephalitis, gingivitis, etc. |
| three | Inflammation involves HOW MANY major processes: mobilization of the body's defenses, containment and destruction of pathogens, and tissue cleanup and repair. |
| hyperemia | The most immediate requirement for dealing with tissue injury is to get defensive leukocytes to the site quickly. The way to do this is local WHAT- increasing blood flow beyond its normal rate. This is achieved by local vasodilation. |
| vasoactive | To bring about hyperemia (dilate blood vessels), certain cels secrete WHAT chemicals that dilate the blood vessels. Among these are histamine, leukotrienes, and other cytokines. These are secreted by basophils of the blood; mast cells of the connective tissue and injured tissue cells |
| capillary permeability | The vasoactive chemicals stimulate endothelial cells of the blood capillaries to separate a little, widening the intercellular clefts between them and increasing WHAT? This allows for the easier movement of fluid, leukocytes, and plasma proteins from the bloodstream into the surrounding tissue (hence swelling) |
| selectins | Endothelial cells of the blood vessels actively aid in the recruitment of leukocytes. In the area of injury, they produce cell-adhesion molecules called WHAT, which make their membranes sticky and snag leukocytes arriving in the blood stream. |
| margination | (inflammation) This adhesion to the vessel wall is called WHAT? |
| diapedesis | The leukocytes then crawl through the gaps between the endothelial cells- an action called wHAT and thus enter the tissue fluid among the cells of the damaged tissue. |
| inflammation | The basis for the four cardinal signs of inflammation: 1. the heat results from the hyperemia 2. Redness is also due to hyperemia 3. swelling (edema) is due to the increased fluid filtration from the capillaries 4. pain results from direct injury to the nerves, pressure on the nerves from the edema, and stimulation of pain receptors by prostaglandins. |
| chemotaxis | The chief enemies of bacteria are neutrophils, which accumulate in the inflamed tissue within an hour of injury. After emigrating from the bloodstream, they exhibit WHAT- attraction to chemicals such as bradykinin and leukotrienes that guide them to the site of injury or infection. |
| monocytes | WHAT are major agents of tissue clean up and repair in inflammation. They emigrate from the bloodstream, and turn into macrophages. Macrophages engulf and destroy bacteria, damaged host cells, and dead and dying neutrophils. They also act as antigen-presenting cells, activating specific immune responses. |
| edema | WHAT also contributes to tissue clean up? (promotes drainage of fluid and debris from site) |
| pus | As the battle progresses, all of the neutrophils and most of the macrophages die. These dead cels, other tissue debris, and tissue fluid form a pool of yellowish fluid called WHAT which accumulates in a tissue cavity called an abscess. |
| platelet-derived growth factor | Blood platelets and endothelial cells in an area of injury secrete WHAT (promotes tissue growth), an agent that stimulates fibroblasts to multiply and synthesize collagen. |
| fever | WHAT is an abnormal elevation of body temperature. It results from trauma, infections, drug reactions, brain tumors, and several other causes. |
| beneficial | Fever is WHAT in that it 1. promotes interferon activity 2. elevates metabolic rate and accelerates tissue repair 3. inhibits reproduction of bacteria and viruses. |
| PGE2 | As neutrophils and macrophages attack fever pathogens, they secrete a variety of chemicals- interleukins, interferons. These chemicals stimulate neurons in the anterior hypothalamus to secrete prostaglandin E2 or wHAT in turn, raises the hypothalamic set point for body temperature- say, to 39C instead of usual 37C. |
| onset | In the stage of fever called WHAT, one has chills, feels cold and clammy to touch, and has a rising temperature |
| stadium | In the next stage of fever, the body temperature oscillates around the new set point for as long as the pathogen is present. |
| defervescence | When the infection is defeated, pyrogen secretion ceases and the hypothalamic thermostat is set back to normal. This activates heat-losing mechanisms, especially vasodilation and sweating. The skin is warm and flushed during this phase. The phase of falling temperature is called WHAT? |
| immune system | The WHAT is composed of a large population of widely distributed cells that recognize foreign substances and act to neutralize or destroy them. |
| specificity | (immune system) Immunity is directed against a particular pathogen. Immunity to one pathogen usually does not confer immunity to others. |
| memory | (immune system) When reexposed to the same pathogen, the body reacts so quickly that there is no noticeable illness. The reaction time for inflammation and other nonspecific defenses, by contrast, is just as long for later exposures as for the initial one. |
| cellular immunity | (cell-mediated) WHAT employs lymphocytes that directly attack and destroy foreign cells or diseased host cells. It is a means of ridding the body of pathogens that reside inside human cells, where they are inaccessible to antibodies: for example, intracellular viruses, bacteria, yeasts, and protozoans. (Attacks foreign cells, diseased host cells. Combats intracellular pathogens, parasites, cancer cells, cells of transplanted tissues) |
| humoral immunity | (antibody-mediated) is mediated by antibodies, which do not directly destroy a pathogen, but tag them for destruction by mechanisms. It is an indirect attack in which antibodies, not the immune cells, assault the pathogen. WHAT is effective against extracellular viruses, bacteria, yeasts, and protozoans against molecular (noncellular) pathogens such as toxins, venoms, and allergens. (Antibodies tag pathogens for destruction by other agents. Combats extracellular pathogens, venoms, toxins, allergens, mismatched RBCs) |
| extracellular | Note that humoral immunity can work only against the WHAT stages of infectious microorganisms. When such microorganisms invade host cells, antibodies cannot get them |
| intracellular stages | WHAT stages are still vulnerable to cellular immunity, which destroys them by killing the cells that harbor them. |
| active immunity | In WHAT, the body makes its own antibodies or T cells against a pathogen |
| passive immunity | In WHAT, the body acquires antibodies or T cells from another person or an animal that has developed its own immunity to the pathogen. |
| natural active immunity | This is the production of one's own antibodies or T cells as a result of natural exposure to an antigen |
| artificial active immunity | This is the production of one's own antibodies or T cells as a result of vaccination against disease. A vaccine consists of either dead or weakened pathogens that can stimulate an immune response but normally cause little or no discomfort or disease. |
| natural passive immunity | This is a temporary immunity that results from acquiring antibodies produced by another person. The only natural ways for this to happen are for a fetus to acquire antibodies from the mother through the placenta before birth, or for a baby to acquire them during breast-feeding. |
| artificial passive immunity | This is a temporary immunity that results from the injection of an immune serum obtained from another person or from animals that produced antibodies against a certain pathogen. |
| antigen | (Ag) WHAT is any molecule that triggers an immune response. Some WHAT are free molecules such as venoms and toxins; others are components of plasma membranes and bacterial cell walls. |
| antigens | WHAT are commonly proteins, polysaccharides, glycoproteins, and glycolipids. Their uniqueness enables the body to distinguish its own "self" molecules from those of any other individual or organism ("nonself"). The immune system "learns" to distinguish self- from nonself-antigens prior to birth; thereafter, it normally attacks only nonself-antigens |
| epitopes | Only certain regions of an antigen molecule, called WHAT, stimulate immune responses. |
| haptens | Some molecules called WHAT, are too small to be antigenic in themselves, but they can stimulate an immune response by binding to a host macromolecule and creating a unique complex that the body recognizes as foreign. |
| immune system | The major cells of the WHAT are lymphocytes, macrophages, and dendritic cells, which are especially concentrated at strategic places such as the lymphatic organs, skin, and mucous membranes. |
| lymphocytes | WHAT fall into 3 classes: NK cells, T lymphocytes, and B lymphocytes |
| red bone marrow | T cells are "born" in the WHAT as descendants of the pluripotent stem cells (PPSCs). The bone marrow releases them into the blood as still-undifferentiated stem cells, which colonize the thymus. |
| thymus | The WHAT is the "school" where they mature into fully functional T cells. In the WHAT cortex, reticular epithelial (RE) cells secrete thymic hormones that stimulate the T cells to develop surface antigen receptors. |
| immunocompetent | With receptors in place, the T cells are now WHAT, capable of recognizing antigens presented to them by APCs. |
| self-antigens | After T cells are immunocompetent, the RE cells then test these T cells by presenting WHAT to them. There are two ways to fail the test: 1. inability to recognize the RE cells at all 2. reacting to self-antigens which means that T cells would attack one's own tissues. |
| negative selection | T cells that fail the test must be eliminated- a process called WHAT. There are two forms of negative selection: clonal deletion and anergy. (98% failing rate) |
| clonal deletion | A type of negative selection of T cells. Self-reactive T cells die and macrophages phagocytize them. |
| anergy | A type of negative selection of T cells. T cells remain alive but unresponsive. |
| self-tolerance | Negative selection leaves the body in a state of WHAT in which the surviving, active T cells respond only to foreign antigens, not to ones's own |
| pass | T cells WHAT the test if they recognize the RE cells but do not react strongly to self-antigens. They now "graduate" to join the immune workforce. Only 2% of the T cells pass their graduation test. |
| positive selection | After T cells pass the test, they move on to the medulla of the thymus, where they undergo WHAT- they multiply and form clones of identical T cells programmed to respond to a particular antigen. These cells, which are immunocompetent but have not yet encountered the "enemy" (foreign antigens), constitute the naive lymphocyte pool. |
| naive lymphocyte pool | The T cells that pass, which are immunocompetent but have not yet encountered the "enemy" (foreign antigens), constitute the WHAT? Naive T cells leave the thymus and colonize lymphatic tissues and organs everywhere in the body (the bone marrow, lymph nodes, tonsils, and so forth); they are now ready to do battle. |
| Life History of a T cell | Life History of a T cell: 1. "born" in the red bone marrow 2. "trained" in Thymus College & State University 3. "employed" in all types of lymphatic tissues and organs. |
| B cells | Another group of fetal stem cells remain in the bone marrow to differentiate into WHAT? Those that respond to self-antigens undergo either anergy or clonal deletion, much like self-reactive T cells. |
| immunocompetent B cell | Self-tolerant B cells go on to produce surface receptors for antigens, divide and produce WHAT clones. These cells disperse throughout the body, colonizing the same organs as T cells. They are abundant in the lymph nodes, spleen, bone marrow, and mucous membranes. |
| antigen-presenting cells | Although the function of T cells is to recognize and attack foreign antigens, they usually cannot recognize such antigens on their own. They require the help of WHAT? |
| major histocompatibility complex | APC function hinges on a family of genes on chromosome 6 called the WHAT? MHC proteins are structurally unique to every person. They act as "identification tags" that label every cell of your body as belonging to you. |
| antigen processing | When an APC encounters an antigen, it internalizes it, digests it, and displays the relevant fragments (its epitopes) in the grooves on its MHC proteins. These steps are called wHAT? |
| nonself-antigen | Wandering T cells regularly inspect APCs for displayed antigens. If an APC displays a self-antigen, the T cells disregard it. If it displays a WHAT, however, the T cells initiate an immune attack |
| APCs | WHAT alert the immune system to the presence of a foreign antigen. The key to a successful defense is then to quickly mobilize immune cells against the antigen. |
| interleukins | Lymphocytes and APCs talk to each other with cytokines called WHAT- chemical signals from one leukocyte to another. |
| Antigen processing by an APC | Antigen processing by an APC: 1. An APC (macrophage) presenting Ag's 2. A helper t cell inspecting the APC |
| cellular immunity | (cell-mediated) WHAT is a form of specific defense in which T lymphocytes directly attack and destroy diseased or foreign cells, and the immune system then remembers the antigens of those invaders and prevents them from causing disease in the future. |
| cellular immunity | WHAT employs four classes of T cells: Cytotoxic T cells, helper T cells, regulatory T cells, and memory T cells |
| cytotoxic T cells | WHAT in cellular immunity are the "effectors" of cellular immunity that carry out the attack on enemy cells. They are also called killer T cells, but are not the same as NK cells |
| helper T cells | WHAT in cellular immunity promote the action of Tc cells as well as playing key roles in humoral immunity and nonspecific resistance. All other T cells are involved in cellular immunity only. |
| regulatory T cells | WHAT in cellular immunity inhibit multiplication and cytokine secretion by other T cells and thus limit immune responses. |
| memory T cells | WHAT in cellular immunity are descended from the cytotoxic T cells and are responsible for memory in cellular immunity |
| three stages of an immune response | three stages of an immune response: 1. Recognition- detect the antigen and recognize it as one the immune system has encountered before 2. Attack- destroy the antigen or the cell harboring it, or mark it for destruction by other means 3. Memory- Remember the antigen so it can be defeated more quickly the next time (before it causes illness) |
| three | Both cellular and humoral immunity occur in HOW MANY stages that we can think of as recognition, attack, and memory (or "the three Rs of immunity"- recognize, react, and remember) |
| recognition | The WHAT phase has two aspects: antigen presentation and T cell activation |
| T cells | When an antigen-presenting cell (APC) encounters and processes an antigen, it typically migrates tot he nearest lymph node and displays it to WHAT? |
| lymph nodes | In Antigen presentation (recognition), cytotoxic and helper T cells patrol the WHAT and other tissues as if looking for trouble. When the cytotoxic and helper T cells encounter a cell displaying an antigen on an MHC protein, they initiate an immune response. T cells respond to two classes of MHC protein: MHC-I proteins and MHC-II proteins |
| MHC-I proteins | WHAT is a kind of class that T cell respond to. It occurs on every nucleated cell of the body. Tc cells respond to WHAT with abnomal Ag's; signify a diseased cell (infected or cancerous) |
| MHC-II proteins | WHAT occur only on APCs and display only foreign antigens. (T helper cells respond to WHAT proteins with foreign Ag's) |
| T cell | WHAT activation begins with a Tc or Th cell binds to an MHCP displaying an epitope that the T cell is programmed to recognize. Before the response can go any further, the T cell must bind to another APC protein, related to interleukins. In a sense, the T cell has to check twice to see if it really has bound to an APC displaying a foreign antigen. |
| costimulation | This signaling process when a T cell checks twice to see if it really has bound to an APC displaying a foreign antigen, called WHAT, helps to ensure that the immune system does not launch an attack in the absence of an ememy. |
| clonal selection | Successful costimulation triggers a process called WHAT? (increasing T cell number). Some cells in the clone become effector cells that carry out an immune attack, and some become memory T cells. |
| interleukins | When a helper T cell recognizes an Ag-MHCP complex, it secretes WHAT that exert three effects: 1. they attract neutrophils and natural killer cells 2. they attract macrophages, stimulate their phagocytic activity, and inhibit them from leaving the area 3. They stimulate T and B cell mitosis and maturation. |
| lethal hit | When a Tc cell recognizes a complex of antigen and MHC-I protein on a diseased or foreign cell, it "docks" on that cell, delivers a WHAT of cytotoxic chemicals that will destroy it. |
| perforin and granzymes | Cytotoxic T cells dock on diseased or foreign cell and secretes a lethal hit of cytotoxic chemicals. These chemicals include WHAT which kill the target cell in the same manner as we saw earlier for NK cells. |
| interferons | Cytotoxic T cells dock on diseased or foreign cell and secretes a lethal hit of cytotoxic chemicals. These chemicals include WHAT which inhibit viral replication and recruit and activate macrophages, among other effects |
| tumor necrosis factor | Cytotoxic T cells dock on diseased or foreign cell and secretes a lethal hit of cytotoxic chemicals. These chemicals include WHAT (TNF) which aids in macrophage activation and kills cancer cells |
| memory T cells | WHAT are long-lived and much more numerous than naive T cells. They also require fewer steps to be activated, and thus respond to antigens more rapidly. |
| T cell recall response | Upon reexposure to the same pathogen later in life, memory cells mount a quick attack called the WHAT. This time-saving response destroys a pathogen so quickly that no noticeable illness occurs- that is, the person is immune to the disease. |
| humoral immunity | WHAT is a more indirect method of defense than cellular immunity. Instead of directly attacking enemy cells, the B lymphocytes of humoral immunity produce antibodies that bind to antigens and tag them for destruction by other means. But like cellular immunity, humoral immunity works in three stages: recognition, attack, and memory. |
| receptor-mediated endocytosis | (recognition in humoral immunity) B cell activation begins when an antigen binds to several of the B cell receptors, links them together, and is taken into the cell by WHAT? |
| MHC-II proteins | (recognition in humoral immunity) After endocytosis, the B cell processes (digests) the antigen, links some of the epitopes to its WHAT and displays these on the cell surface. |
| interleukins | (recognition in humoral immunity) Usually, the B cell response goes no further unless a helper T cell binds to this Ag-MHCP complex. (Some B cells are directly activated by antigens without the help of a Th cell). When a Th cell does bind to the complex, it secretes WHAT that activate the B cell. |
| clonal selection | (recognition in humoral immunity) When a Th cell does bind to the complex, it triggers WHAT- of B cells giving rise to a battalion of identical B cells programmed against the same antigen. |
| plasma cells | (recognition in humoral immunity) Most of the cells of the clone differentiate into WHAT? These are larger than B cells and contain an abundance of rough ER. A WHAT cell secretes antibodies. |
| Events of the Humoral Immune Response | Events of the Humoral Immune Response: 1. Antigen recognition 2. Antigen presentation 3. clonal selection 4. Differentiation 5. Attack (p. 845) |
| immunoglobulin | (Ig) WHAT is an antibody that is a defensive gamma globulin found in the blood plasma, tissue fluids, body secretions, and some leukocyte membranes. |
| antibody monomer | The basic structural unity of an antibody, a WHAT is composed of four polypeptides linked by disulfide (-S-S-) bonds. The two larger heavy chains are about 400 amino acids long, and the two light chains about half that long. Each heavy chain has a hinge region where the antibody is bent, giving the monomer a T or Y shape. |
| variable region | All four chains of antibodies have a WHAT that gives an antibody its uniqueness. |
| antigen-binding site | The V regions of antibodies of a heavy chain and light chain combine to form an WHAT on each arm, which attaches to the epitope of an antigen molecule. |
| constant region | The rest of each chain of antigen is a WHAT? The C region determines the mechanism of an antibody's action- ex.) whether it can bind complement proteins |
| five | There are HOW MANY classes of antibodies named IgA, IgD, IgE, IgG, and IgM named for the structures of their C regions. |
| IgD and IgM | The surface antigen receptors synthesized by a developing B cell are WHAT and WHAT molecules. |
| IgG | WHAT antibody is particularly important int he immunity of the newborn because it crosses the placenta with relative ease. Thus, it transfers immunity from the mother to her fetus. |
| IgA | An infant acquires some maternal WHAT antibody through breast milk and colostrum. |
| four | Once released by a plasma cell, antibodies use HOW MANY mechanism to render antigens harmless: neutralization, complement fixation, agglutination, precipitation. *Antibodies do not directly destroy an antigen in any of these mechanisms |
| neutralization | (mechanism that antibodies use to render antigens harmless) Only certain regions of an antigen are pathogenic. Antibodies can neutralize an antigen by masking these active regions. |
| complement fixation | (mechanism that antibodies use to render antigens harmless) Antibodies IgM and IgG bind to enemy cells and change shape, exposing their complement-binding sites. This initiates the binding of complement to the enemy cell surface and leads to inflammation, phagocytosis, immune clearance, and cytolysis. WHAT is the primary mechanism of defense against such foreign cells as bacteria and mismatched erythrocytes |
| agglutination | (mechanism that antibodies use to render antigens harmless) It is effective not only in mismatched blood transfusions, but more importantly as a defense against bacteria. An antibody molecule has 2 to 10 binding sites; thus, it can bind to antigen molecules on two or more enemy cells at once and stick them together. This immobilizes microbes and antigen molecules and prevents them from spreading through the tissues |
| precipitation | (mechanism that antibodies use to render antigens harmless) It is a similar process in which antibodies link antigen molecules together. This creates large Ag-Ab complexes that are too large to remain dissolved in solution. These complexes can be removed by immune clearance or phagocytized by eosinophils in the connective tissues. |
| primary response | When a person is exposed to a particular antigen for the first time, the immune reaction is called the WHAT? |
| antibody titer | As the plasma cells begin secreting antibody, the WHAT (level in the blood plasma) begins to rise. (primary response). IgM appears first, peaks in about 10 days, and soon declines. IgG levels rise as IgM declines, but even the IgG titer drops to a low level within a month. |
| memory B cells | The primary response leaves one with an immune memory of the antigen. During clonal selection, some members of the clone become WHAT rather than plasma cells. |
| anamnestic | Memory B cells mount a very quick secondary or WHAT response if reexposed to the same antigen. Plasma cells form within hours, so the IgG titer rises sharply and peaks within a few days. The response is so rapid that the antigen has little chance to exert a noticeable effect on the body, and no illness results. A low level of IgM is also secreted and quickly declines, but IgG remains elevated for weeks to years, conferring lasting protection |
| memory | WHAT does not last as long in humoral immunity, however, as it does in cellular immunity. |
| hypersensitivity | WHAT is an excessive, harmful immune reaction to antigens that most people tolerate. It includes reactions to tissues transplanted from another person (alloimmunity), abnormal reactions to one's own tissues (autoimmunity) and allergies, which are reactions to environmental antigens. |
| Type I hypersensitivity | (acute) WHAT includes the most common allergies. WHAT is an IgE-mediated reaction that begins within seconds of exposure. Some examples are food allergies and asthma. (response is very rapid) |
| Anaphylaxis | WHAT is an immediate and severe type I reaction. WHAT shock is a severe, widespread acute hypersensitivity that occurs when an allergen such as bee venom or penicillin is introduced to the bloodstream of an allergic individual. It is characterized by bronchoconstriction, dyspnea (labored breathing), widespread vasodilation, circulatory shock. |
| Type II hypersensitivity | (antibody-dependent cytotoxic) WHAT occurs when IgG or IgM attacks antigens bound to cell surfaces. The reaction leads to complement activation and either lysis or opsonization of the target cell. Macrophages phagocytize and destroy opsonized platelets, erythrocytes, or other cells. Examples of cell destruction by WHAT reactions are blood transfusion reactions, and some drug reactions. |
| Type III hypersensitivity | (immune complex) WHAT occurs when IgG or IgM forms antigen-antibody complexes that precipitate beneath the endothelium of the blood vessels or in other tissues. These complexes activate complement and trigger intense inflammation, causing tissue destruction. Two ex. are the autoimmune disease acute glomerulonephritis and systemic lupus erythrematosus, a widespread inflammation of the connective tissues. (slower onset) |
| Type IV hypersensitivity | (delayed) what is a cell-mediated reaction in which the signs appear about 12 to 72 hours after exposure. It begins with APCs in the lymph nodes display antigens to helper T cells, and these T cells secrete interferon and other cytokines that activate cytotoxic T cells and macrophages. Ex.) include allergies to haptens in cosmetics and poison ivy; graft rejection; the tuberculosis skin test. (delayed cell-mediated response) |
| I-III | Types WHAT are antibody-mediated |
| IV | Type WHAT is cell-mediated |
| I | Type WHAT is acute (immediate onset) |
| II-III | Types WHAT are subacute (onset usually in 1-3 hours) |
| autoimmune diseases | WHAT are failures of self-tolerance-- the immune system fails to distinguish self-antigens from foreign ones and produces autoantibodies that attack the body;s own tissues |
| cross-reactivity | (autoimmune disease) (reason why self-tolerance may fail) Some antibodies against foreign antigens react to similar self-antigens. Ex.) In rheumatic fever, a stroptococcus infection stimulates production of antibodies that react not only against the bacteria but also against antigens of the heart tissue. |
| abnormal exposure of self-antigens to blood | (autoimmune disease) (reason why self-tolerance may fail) Some of our native antigens are normally not exposed to the blood. Ex.) blood-testis barrier (BTB) normally isolates sperm cells from the blood. Breakdown of the BTB can cause sterility when sperm first form in adolescence and activate the production of autoantibodies. |
| change in the structure of self-antigens | (autoimmune disease) (reason why self-tolerance may fail) Viruses and drugs may change the structure of self-antigens and cause the immune system to perceive them as foreign. Ex.) Type I diabetes mellitus |
| severe combined immunodeficiency disease | (SCID) WHAT is a group of disorders caused by recessive alleles that result in a scarcity or absence of both T and B cells. Children with SCID are highly vulnerable to opportunistic infections and must live in protective enclosures. David Vetter, who spent his life in sterile plastic chambers and suits, finally died at age 12 to cancer triggered by a viral infection. David contacted the fatal virus from his sister through a borne marrow transplant. |
| acquired immunodeficiency syndrome | (AIDS) A group of conditions that involve a severely depressed immune response caused by infection with the human immunodeficiency virus (HIV) |
| structure of HIV | structure of HIV: Its inner core consists of a protein capsid enclosing two molecules of RNA, two molecules of an enzyme called reverse transcriptase, and a few other enzyme molecules. The capsid is enclosed in another layer of viral protein, the matrix. External to this is a viral envelope composed of phospholipids and glycoproteins derived from the host cell. |
| HIV | WHAT can be replicated only by a living host cell. It invades helper T cells, dendritic cells, and macrophages. HIV adheres to a target cell by "tricking" the target cell into internalizing it by receptor-mediated endocytosis (a process by which cells absorb molecules (such as proteins) by engulfing them). Within the host cell, reverse transcriptase uses the viral RNA as a template to synthesize DNA. Viruses that carry out this RNA->DNA reverse transcription are called retroviruses. The new DNA is inserted into the host cell's dNA, where it may lie dormant for months to years. As the new viruses emerge from the host cell, they are coated with bits of the cell's plasma membrane, forming the new viral envelope. The new viruses then adhere to more host cells and repeat the process. |
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