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47 Cards in this Set
- Front
- Back
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•Immune system has twointrinsic systems |
•Innate (nonspecific) defense system •Adaptive (specific) defense system |
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1.Innatedefense system has two lines of defense |
•First line of defense is externalbody membranes (skin and mucosae) •Second line of defense isantimicrobial proteins, phagocytes, NK cells and other cells •Inhibit spread of invaders •Inflammation is its mostimportant mechanism |
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Adaptive defense system
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•Third line of defense attacks particular foreign substances •Takes longer to react than the innate system •Innate and adaptivedefenses are deeply intertwined |
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(Innate Defenses) Surface barriers
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•Skin, mucous membranes, and their secretions •Physical barrier to most microorganisms •Keratin is resistant to weak acids and bases, bacterialenzymes, and toxins •Mucosaeprovide similar mechanical barriers |
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Protective chemicals that inhibit or destroy microorganisms
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•Skin acidity •Lipids in sebum and dermcidin insweat •HCl andprotein-digesting enzymes of stomach mucosae •Lysozyme ofsaliva and lacrimal fluid •Mucus |
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respiratory system modifications
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•Mucus-coated hairs in the nose •Cilia of upper respiratory tract sweep dust- and bacteria-ladenmucus from lower respiratory passages |
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Internal Defenses: Cellsand Chemicals |
•Necessaryif microorganisms invade deeper tissues •Phagocytes •Natural killer (NK) cells •Inflammatory response(macrophages, mast cells, WBCs, and inflammatory chemicals) •Antimicrobial proteins (interferons and complement proteins) Fever |
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Macrophages
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•Macrophagesdevelop from monocytes tobecome the chief phagocytic cells •Free macrophages wander throughtissue spaces •E.g., alveolar macrophages •Fixed macrophages are permanentresidents of some organs •E.g., Kupffer cells (liver) and microglia(brain) |
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•Phagocytes: Neutrophils •Neutrophils •Become phagocytic on encountering infectious material intissues • |
•Neutrophils •Become phagocytic on encountering infectiousmaterial in tissues |
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Events of phagocytosis
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1.)Phagocyte asheres to pathogens or debris 2.) Phagocyte fors pseudopods that eventually engulf the particles forming a phagosome 3.) Lysosome fuses with the phagocytic vesicle, forming a phagolysosome 4.) Lysosomal enzymes digest the paticles leaving a residual body 5.) exocytosis of the vesicle removes indigestible and residual material. |
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•Mechnism of phagocytosis |
•Destructionof pathogens •Acidification and digestion by lysosomal enzymes •Respiratory burst •Release of cell-killing freeradicals •Activation of additional enzymes •Oxidizing chemicals (e.g. H2O2) •Defensins (in neutrophils) |
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•Natural Killer (NK) Cells |
•Large granular lymphocytes •Target cells that lack“self” cell-surface receptors •Induce apoptosis in cancercells and virus-infected cells •Secrete potent chemicalsthat enhance the inflammatory response |
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Inflammatory Response
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•Triggered whenever bodytissues are injured or infected •Prevents the spread ofdamaging agents •Disposes of cell debrisand pathogens •Sets the stage for repair |
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•Cardinal signs of acuteinflammation: |
1.Redness 2.Heat 3.Swelling 4.Pain (And sometimes 5. Impairment of function |
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Macrophages and epithelialcells of boundary tissues
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bear Toll-like receptors(TLRs)
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TLRS
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•recognize specific classesof infecting microbes Activated TLRs trigger the release ofcytokines that promote inflammation |
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Inflammatory Mediators
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•Histamine (from mast cells) •Blood proteins •Kinins,prostaglandins (PGs), leukotrienes, and complement •Released by injured tissue, phagocytes, lymphocytes, basophils, and mast cells |
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Inflammatory Chemicals cause |
•Dilation of arterioles, resulting in hyperemia •Increased permeability of local capillaries and edema (leakageof exudate) •Exudate contains proteins, clotting factors, andantibodies |
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•Functions of the surge of exudate |
•Moves foreign material into lymphatic vessels •Delivers clotting proteins to form a scaffold for repair and toisolate the area |
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Phagocyte mobilization
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•Neutrophils, then macrophages flood to inflamed sites |
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Steps of phagocyte mobilization
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1.Leukocytosis:release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injuredcells 2.Margination:neutrophils cling to the walls ofcapillaries in the inflamed area 3.Diapedesisof neutrophils 4.Chemotaxis:inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils |
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Antimicrobial Proteins (Interferons (IFNS) and complement proteins
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•Attack microorganisms directly •Hinder microorganisms’ ability to reproduce |
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Interferons
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•Viral-infected cells areactivated to secrete IFNs •IFNs enter neighboringcells •Neighboring cells produceantiviral proteins that block viral reproduction |
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Produced by a variety of body cells (interferons)
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•Lymphocytes produce gamma (g), or immune, interferon •Most other WBCs produce alpha (a) interferon •Fibroblasts produce beta (b) interferon •Interferonsalso activate macrophages and mobilize natural killer cells |
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Interferon (functions)
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•Anti-viral •Reduce inflammation •Activate macrophages and mobilizeNK cells •Geneticallyengineered IFNs for •Antiviral agents againsthepatitis and genital warts virus •Multiple sclerosis treatment |
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Complement
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•~20 blood proteins that circulate in an inactiveform •Include C1–C9, factors B,D, and P, and regulatory proteins •Major mechanism fordestroying foreign substances |
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Complement Functions
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•Amplifies all aspects ofthe inflammatory response •Kills bacteria and certainother cell types by cell lysis •Enhances both nonspecificand specific defenses |
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Complement Activation (Classical)
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1.Classical pathway •Antibodies bind to invadingorganisms •C1 binds to the antigen-antibodycomplexes (complement fixation) |
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Complement Activation (Alternative)
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•Triggered when activated C3, B,D, and P interact on the surface of microorganisms |
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pathways in Complement Activation
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•Each pathway involvesactivation of proteins in an orderly sequence •Each step catalyzes thenext •Both pathways converge onC3, which cleaves into C3a and C3b |
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Activated Complement
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•Enhances inflammation •Promotes phagocytosis •Causes cell lysis •C3b initiates formation of amembrane attack complex (MAC) •MAC causes cell lysis by inducing a massive influx ofwater •C3b also causes opsonization, and C3a causes inflammation |
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Fever
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•Systemic response toinvading microorganisms •Leukocytes and macrophagesexposed to foreign substances secrete pyrogens •Pyrogens reset the body’s thermostat upward |
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Benefits of moderate Fever
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•Causes the liver and spleen to sequester iron and zinc (neededby microorganisms) •Increases metabolic rate, which speeds up repair **High Fevers are dangerous because heat denatures enzymes** |
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Adaptive Defenses
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•The adaptive immune(specific defense) system •Protects against infectious agents and abnormal body cells •Amplifies the inflammatory response •Activates complement |
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Adaptive immune response
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•Is specific •Is systemic •Has memory |
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Adaptive defenses (2 seperate overlapping arms)
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1.Humoral(antibody-mediated) immunity 2.Cellular (cell-mediated) immunity |
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Antigens
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•Substances that canmobilize the adaptive defenses and provoke an immune response Most are large, complex molecules notnormally found in the body (nonself |
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Immunogenicity
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the ability to stimulatespecific lymphocytes to proliferate (multiply)
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Reactivity
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the ability to reactwith the lymphocytes and the antibodies released immunogenic reactions
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Complete Antigens (Important functional properties)
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•Examples: foreign protein,polysaccharides, lipids, and nucleic acids |
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Haptens (Incomplete Antigens)
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•Smallmolecules (peptides, nucleotides, and hormones) •Notimmunogenic by themselves •Areimmunogenic when attached to body proteins •Causethe immune system to mount a harmful attack •Examples:poison ivy, animal dander, detergents, and cosmetics |
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Antigenic Determinants
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•Certain parts of an entireantigen that are immunogenic •Antibodies and lymphocytereceptors bind to them |
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•Most naturally occurringantigens have numerous antigenic determinants that |
•Mobilize several different lymphocyte populations •Form different kinds of antibodies against it. •Large, chemically simple molecules (e.g.,plastics) have little or no immunogenicity |
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Self Antigens: MHC Proteins
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•Protein molecules(self-antigens) on the surface of cells •Antigenic to others intransfusions or grafts •Example: MHC proteins •Coded for by genes of the major histocompatibility complex (MHC) and are unique to an individual •MHC proteins displaypeptides (usually self-antigens) •In infected cells, MHCproteins display fragments of foreign antigens, which help mobilize the immuneresponse |
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Class I MHC Proteins
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Found on virtually all body cells
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Class II MHC proteins
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Found only on certain cells that act in the immune response.
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