Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
•Immune system has twointrinsic systems |
•Innate (nonspecific) defense system •Adaptive (specific) defense system |
|
1.Innatedefense system has two lines of defense |
•First line of defense is external body membranes (skin and mucosae) •Second line of defense is antimicrobial proteins, phagocytes, NK cells and other cells •Inhibit spread of invaders -Inflammation is its most important mechanism •Inflammation is its mostimportant mechanism |
|
Adaptive defense system
|
•Third line of defense attacks particular foreign substances •Takes longer to react than the innate system •Innate and adaptivedefenses are deeply intertwined |
|
(Innate Defenses) Surface barriers
|
•Skin, mucous membranes, and their secretions •Physical barrier to most microorganisms •Keratin is resistant to weak acids and bases, bacterial enzymes, and toxins •Mucosae provide similar mechanical barriers |
|
Protective chemicals that inhibit or destroy microorganisms
|
•Skin acidity •Lipids in sebum and dermcidin insweat •HCl andprotein-digesting enzymes of stomach mucosae •Lysozyme ofsaliva and lacrimal fluid •Mucus |
|
respiratory system modifications
|
•Mucus-coated hairs in the nose •Cilia of upper respiratory tract sweep dust- and bacteria-ladenmucus from lower respiratory passages |
|
Internal Defenses: Cells and Chemicals |
• Necessary if 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 |
|
Macrophages
|
•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) |
|
Neutrophils |
•Become phagocytic on encountering infectiousmaterial in tissues |
|
Events of phagocytosis
|
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. |
|
•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) |
|
•Natural Killer (NK) Cells |
•Large granular lymphocytes •Target cells that lack“self” cell-surface receptors •Induce apoptosis in cancer cells and virus-infected cells •Secrete potent chemicalsthat enhance the inflammatory response |
|
Inflammatory Response
|
•Triggered whenever bodytissues are injured or infected •Prevents the spread ofdamaging agents •Disposes of cell debrisand pathogens •Sets the stage for repair |
|
•Cardinal signs of acute inflammation: |
1.Redness 2.Heat 3.Swelling 4.Pain (And sometimes 5. Impairment of function |
|
Macrophages and epithelialcells of boundary tissues
|
bear Toll-like receptors(TLRs)
|
|
TLRS
|
•recognize specific classes of infecting microbes Activated TLRs trigger the release ofcytokines that promote inflammation |
|
Inflammatory Mediators
|
•Histamine (from mast cells) •Blood proteins •Kinins,prostaglandins (PGs), leukotrienes, and complement •Released by injured tissue, phagocytes, lymphocytes, basophils, and mast cells |
|
Inflammatory Chemicals cause |
•Dilation of arterioles, resulting in hyperemia •Increased permeability of local capillaries and edema (leakageof exudate) •Exudate contains proteins, clotting factors, and antibodies |
|
•(Inflammatory response EDEMA) 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 |
|
Steps of phagocyte mobilization
|
•Neutrophils, then macrophages flood to inflamed sites 1.Leukocytosis:release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells 2.Margination:neutrophils cling to the walls ofcapillaries in the inflamed area 3.Diapedesis of neutrophils 4.Chemotaxis:inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils |
|
Antimicrobial Proteins (Interferons (IFNS) and complement proteins
|
•Attack microorganisms directly •Hinder microorganisms’ ability to reproduce |
|
Interferons
|
•Viral-infected cells areactivated to secrete IFNs •IFNs enter neighboringcells •Neighboring cells produceantiviral proteins that block viral reproduction |
|
Produced by a variety of body cells (interferons)
|
•Lymphocytes produce gamma (g), or immune, interferon •Most other WBCs produce alpha (a) interferon •Fibroblasts produce beta (b) interferon •Interferons also activate macrophages and mobilize natural killer cells |
|
Interferon (functions)
|
•Anti-viral •Reduce inflammation •Activate macrophages and mobilizeNK cells •Genetically engineered IFNs for •Antiviral agents against hepatitis and genital warts virus •Multiple sclerosis treatment |
|
Complement
|
•~20 blood proteins that circulate in an inactiveform •Include C1–C9, factors B,D, and P, and regulatory proteins •Major mechanism for destroying foreign substances |
|
Complement Functions
|
•Amplifies all aspects ofthe inflammatory response •Kills bacteria and certainother cell types by cell lysis •Enhances both nonspecificand specific defenses |
|
Complement Activation
|
Activated Complement Enhances Inflammation Promotes Phagocytosis Causes Cell Lysis |
|
Fever
|
•Systemic response toinvading microorganisms •Leukocytes and macrophages exposed to foreign substances secrete pyrogens •Pyrogens reset the body’s thermostat upward |
|
Benefits of moderate Fever
|
•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** |
|
Adaptive Defenses
|
•The adaptive immune(specific defense) system •Protects against infectious agents and abnormal body cells •Amplifies the inflammatory response •Activates complement |
|
Adaptive immune response
|
•Is specific •Is systemic •Has memory |
|
Adaptive defenses (2 seperate overlapping arms)
|
1.Humoral(antibody-mediated) immunity 2.Cellular (cell-mediated) immunity |
|
Antigens
|
•Substances that can mobilize the adaptive defenses and provoke an immune response Most are large, complex molecules notnormally found in the body (nonself) |
|
Immunogenicity
|
the ability to stimulate specific lymphocytes to proliferate (multiply)
|
|
Reactivity
|
the ability to react with products of activated lymphocytes and antibodies released.
|
|
Complete Antigens (Important functional properties)
|
•Examples: foreign protein,polysaccharides, lipids, and nucleic acids |
|
Haptens (Incomplete Antigens)
|
•Smallmolecules (peptides, nucleotides, and hormones) •Not immunogenic by themselves •Are immunogenic when attached to body proteins •Cause the immune system to mount a harmful attack •Examples:poison ivy, animal dander, detergents, and cosmetics |
|
Antigenic Determinants
|
•Certain parts of an entireantigen that are immunogenic •Antibodies and lymphocytereceptors bind to them |
|
•Most naturally occurring antigens 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 |
|
Self Antigens: MHC Proteins
|
•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 |
|
Class I MHC Proteins
|
Found on virtually all body cells
|
|
Class II MHC proteins
|
Found only on certain cells that act in the immune response.
|
|
Opsonization
|
Coating of pathogen by complement proteins or antibodies
|