Unit 4 – Microbiology Test Questions – Flashcards
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| Portals of Entry for Microbial Infection |
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| Respiratory Tract Genitourinary Tract (GU) Gastrointestinal (GI) Skin Parenteral Route (Insect Bites) Placenta |
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| Invasiveness |
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| The ability of a microbe to colonize the tissues of a host. Some bacteria have structural components which act as adhesions/ligands and bind to receptors on host cells- can form biofilms Examples: Capsule- Streptococcus mutans Fimbriae- Escherichia coli M Protein (wall)- Streptococcus pyogenes Opa protein (wall)- Neisseria gonorrhoeae Mycolic acid (wall)- Mycobacterium tuburculosis A protein (wall)- A protein which binds antiodies by stem region- Staphococcus aureus Some bacteria use structural components to protect themselves from phagocytosis: Capsules & Cell Wall Proteins |
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| Toxicity |
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| The ability of a microbe to produce a harmful substance such as an exotoxin or endotoxin. |
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| Capsules |
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| Prevent phagocytosis -Streptococcus pneumoniae -Haemophilus influenzae -Bacillus anthracis |
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| Cell Wall Components |
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| M Protein- resists phagocytosis (streptococcus pyogenes) Opa protein- inhibits T helper cells (Neisseria gonorrhoeae) Mycolic acid (waxy lipid)- resists digestion (Mycobacterium tuberculosis) A protein- Staph. aureus has a protein associated with the wall; "A-protein" which binds antibodies by the stem region. |
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| Toxin |
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| Substance that contributes to pathogenicity. |
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| Toxigenicity |
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| Ability to produce a toxin |
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| Toxemia |
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| Presence of toxin in the host's blood. |
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| Toxoid |
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| Inactivated toxin used in a vaccine. |
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| Antitoxin |
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| Antibodies against a specific toxin |
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| Membrane-Disrupting Toxins |
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| Lyse host's cells by- 1. Making protein channels in the plasma membrane (leukocidins, hemolysins (alph & beta), streptolysins 2. Disrupting phospholipid bilayer. |
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| Superantigens |
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| Cause an intense immune response due to release of cytokines from host cells. Symptoms: fever, nausea, vomiting, diarrhea, shock and death |
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| Endotoxins and the Pyrogenic Response |
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| 1. A macrophage ingests a gram-negative bacterium. 2. The bacterium is degraded in a vacuole, releasing endotoxins that induce the macrophage to produce cytokines IL-1 & TNF-alpha 3. The cytokines are released into the bloodstream by the macrophages, through which they travel to the hypothalamus of the brain. 4. The cytokines induce the hypothalamus to produce prostaglandins, which reset the body's "thermostat" to a higher temp, producing fever. |
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| Enzymes Produced as Virulance Factors |
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| Hyaluronidase, Kinases, Coagulases, Collagenase, Ig-A proteases, Keritinase |
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| Hyaluronidase |
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| called the "spreading factor"- breaks down hyaluronic acid, a tissue "cement" found particularly in connective tissue |
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| Kinases |
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| enzymes that dissolve fibrin clots formed in tissue in response to trauma allowing organisms to invade |
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| Coagulases |
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| enzymes that initiate clot formation (fibinogen->fibrin) in plasma walls off organisms and prevents phagocytosis. (Staph. aureus) |
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| Collagenase |
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| an enzyme which breaks down collagen, a binding protein found in connective tissue throughout the body. (Gang green) |
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| Ig-A Proteases |
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| destroy IgA (mucosal antibody) antibodies |
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| Keratinase |
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| digest keratin- protein found in skin and nails |
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| Exotoxins |
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| Proteins produced inside pathogenic bacteria, most commonly G+ bacteria, as part of their growth & metabolism. They are then secreted or released into the surrounding medium following lysis. Heat sensitive; strongly anitigenic (immunize w/taxoid); can be classified by action; highly toxic. A-B (diptheria & botulism)- inhibit protein synthesis) Membrane Disruption- Hemolysins & Leukocidins Superantigens- Staph. enterotoxin (in gut) Symptoms: fever, cardiovascular disturbances, diarrhea & shock. (vary by which type) |
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| Endotoxins |
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| The lipid portions of lipopolysaccharides (LPSs) that are part of the outer membrane of the cell wall of G- (Lipid A). They are liberated when the bacteria die and the cell wall breaks apart during lysis. Stimulate macrophages to release cytokines in very high, toxic concentrations. Heat resistent; non-specific generalized action; weak antigen (antibodies are nonprotective, therefor, no toxoid); no antitoxin, but drug "Zovan" counteracts clotting & inflammation Responsible for meningococcal meningitis & typhoid fever Symptoms: chills, fever, weakness, generalized aches & in some cases, shock & death. Can also induce miscarriages. |
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| Innate Immunity |
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| immunity that is present at birth. |
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| First line of defense |
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| Intact skin Mucous membranes and their secretions Normal Microbiota |
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| Second line of defense |
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| Phagocytes, such as neutrophils, eosinophils, dendritic cells and macrophages Inflammation Fever Antimicrobial substances |
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| Adaptive Immunity (3rd line of defense) |
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| Specialized lymphocytes: T cells & B cells Antibodies |
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| Cytokines |
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| proteins that regulate the intensity and duration of immune responses; recruit other macrophages & dendritic cells to isolate & destroy microbes as part of the inflammatory response; also activate T cells & B cells in adaptive immunity |
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| Innate Immunity (function) |
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| Toll-like receptors (TLRs) attach to Pathogen-associated Molecular Patterns (PAMPs) and induce cytokines that regulate the intensity & duration of the immune response. |
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| Mechanical Defenses in Innate Immunity |
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| Skin- epithelial barrier, keratin Respiratory Tract- epithelial barrier; mucous membrane; cilia; haris in nares; coughing; sneezing Gastrointestinal Tract- epithelial layer' mucous membranes; peristalsis (smooth muscle contraction) Genitourinary Tract- epithelial barrier; mucous membranes; urine flow; length of urethra & ureters; cervical barrier; vaginal secretions |
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| Chemical Defenses in Innate Immunity |
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| Skin- fatty acids in sebum; low pH; low moisture; high salt; lysozome; interferons Respiratory Tract- lysozome; salt in tears; interferons Gastrointestinal Tract- low pH; bile salts; gastric juices; lysozome; interferons Genitourinary Tract- low pH; interferons |
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| Cellular Defense Mechanisms |
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| Phagocytosis Normal Microbiota Inflammation Fever Interferons |
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| Phagocytosis |
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| the ingestion of a microorganism or substance (such as debris) by a cell. Process: chemotaxis (chemical attraction)->Ingestion of microbe by phagocyte->Digestion of ingested microbe by enzymes (lysosome)-> Discharge of waste materials |
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| Inflammation |
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| Function- Destruction of pathogen, confinement of injured area, repair of injured tissue Triggers- injury to host tissue Responsible Cells- basophils, mast cells & platelets Signs: redness, swelling, pain, heat Stages: vasodilation & increased permeability in blood vessels; phagocyte migration & phagocytosis; repair Chemicals released: Histamine, Kinins, Prostaglandins, Leukotrienes |
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| Fever |
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| ADVANTAGES: Increases transferrins, decreasing iron available to microbes Increases IL-1 activity, thus increasing T-cell production Intensifies Interferon Increases metabolic rate which may help w/body reactions or hurt w/acidosis Slows growth of some pathogens, but will NOT kill bacteria DISADVANTAGES: Tachycardia Acidosis (metabolizing fat instead of sugar) Dehydration 44-46 degrees is fatal |
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| Interferons |
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| Proteins produced in small amounts by specific host cells (host specific, not virus specific). Types- Alpha, Beta & Gamma "Paul Revere" cytokines that warn that a virus is present. Newly warned neighbor cell then produces anti-viral proteins (AVPs) which interfere with viral replication. |
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| Complement System |
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| defensive system consisting of over 30 serum proteins found in normal serums. |
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| What activates the 3 compliment pathways? |
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| 1. Antigen Antibody Complex 2. Chemical complexes on the surface of foreign cells. 3. Lectins- proteins produced by the liver |
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| What are the actions of complement? |
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| 1. Opsonization or immune adherence (enhanced phagocytosis) 2. Membrane attack complex (cytolysis) 3. Attract phagocytes (Stimulate inflammation) |
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| Neutrophils |
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| Phagocytosis (70% of white blood cells) |
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| Basophils |
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| (mast cells) Produce inflammatory chemicals: histamine, leucotrienes, prostaglandins |
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| Eosinophils |
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| Produces toxic proteins against certain parasites, some phagocytosis Numbers increase during an allergic response. |
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| Dendritic Cells |
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| Derived from monocytes; phagocytosis and initiation of adaptive immune response- APC (anitgen presenting cells) |
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| Monocytes |
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| phagocytic as mature microphages- APC |
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| Lymphocytes |
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| NK (natural killer cells)- Lymphocite cells without T or B cell markers that are NOT antigen specific. They have receptors for the Fc region of IgG antibodies. When they detect a cell with numerous IgG antibodies attached they attack it in the manner of the CD_8 cytotoxic cell using perforin and proteases to induce apoptosis. This is called antibody-dependent cell mediated cytotoxicity (ADCC). This is usefull in controlling large parasites too large to be engulfed by phagocytic cells. Involved in adaptive immunity. |
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| Chemicals Released by damaged cells |
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| Histamine- vasodilation, increased permeability of blood vessels Kinins- Vasodilation, increased permeability of blood vessels Prostaglandins- Intensity histamine and kinin effect Leukotrienes- Increased permeability of blood vessels, phagocytic attachment |
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| Opsonization |
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| The enhancement of phagocytosis by coating microorganisms with certain serum proteins (opsonins); also called immune adherence |
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| IgM |
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| 1st responder; pentamer |
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| IgA |
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| in secretions; dimer |
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| IgE |
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| allergic reactions; worms |
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| IgG |
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| 80% of serum antibodies; able to cross placenta & found in breast milk |
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| T cells |
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| Cell-mediated immunity |
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| B cells |
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| Descendents of B cells (plasma cells)- produce antibodies |
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| T-lymphocytes |
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| mature in thymus; can be divided into 2 major subsets- CD4+ (helpers) & CD8+(cytotoxic) |
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| CD-4 cells |
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| also known as TH or T-helper cells; once activated by antigen exposure they differentiate into 2 populations- TH-1s & TH-2s. |
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| TH-1 |
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| produce cytokines that activate macrophages, stimulate production of antibodies that promote phagocytosis & enhance complement; activates eosinophils. |
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| TH-2 |
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| produce cytokines that are primarily associated with antibody production, especially IgM & IgE; activates eosinophils. |
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| CD-8 cells |
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| activated by dendritic cells & TH-1 cells to become CTLs (cytotoxic T lymphocyte), which release cytotoxins such as perforin and proteases. Perforin facilitates penetration of proteases called granzymes which induce apoptosis in the target cell- an abnormal host cell causing its death by minimizing inflammation or spread of a virus to other cells. |
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| T-regulatory cells |
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| appear to suppress other T-cells, secrete IL-10 and regulate the immune response. They combat autoimmunity and protect the intestinal bacteria from the immune system. They are a subset of the CD-4 cells and also carry the CD-25 marker. |
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| Superantigens |
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| relatively nonspecific antigens that indiscriminately activate many T-cell receptors at once, producing a response harmful to the host. Examples of such antigens are the enterotoxins of Staphylococcus aureus and the toxin of toxic shock syndrome. |
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| Cytokines |
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| a small protein released from human cells that regulates the immune response; directly or indirectly may induce fever, pain or T-cell proliferation. |
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| Lysosome |
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| an organelle containing digestive enzymes |
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| Active Immunity |
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| when a person is exposed to microorganisms or foreign substances and the immune system responds. |
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| Passive Immunity |
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| when antibodies are transferred from one person to another. Only lasts as long as the antibodies are present- in most cases, a few weeks. |
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| Antiserum |
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| A blood-derived fluid containing antibodies. |
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| M (microfold) cells |
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| Intestinal cells that take up and transfer antigens to lymphocytes. |
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| Haptens |
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| A substance of low molecular weight that does not cause the formation of antibodies by itself, but does so when combined with a carrier molecule. |
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| Clonal Selection |
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| The development of clones B and T cells against a specific antigen. |
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| Apoptosis |
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| The natural programmed death of a cell; the residual fragments are disposed of by phagocytosis. |
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| Hypersensitivity |
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| An altered, enhanced immune reaction leading to pathological changes; also called allergy |
