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Micro > Week 9 Exam 3 > Flashcards

Week 9 Exam 3 Flashcards

1
Q

immunology

A
  • study of the body’s 2nd and 3rd lines of defense
  • study of the body’s response to infectious agents
  • study of allergies and cancer
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2
Q
  • immunity:
  • immune function:
  • wbcs:
A

-immunity: ability to ward off disease. it is carried out by a network of cells and fluids in every tissue and organ
-healthy immune system will:
provide surveillance
recognize foreign material
destroy entities deemed to be foreign
-WBCs:
recognize body cells: self
differentiate them from foreign material: non-self
-ability to evaluate macromolecules as self or non self is central to the functioning of the IS
-autoimmune disorders are the result of the body attacking its self

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3
Q

Lymphatic system & lymph

A
  • made up of lymphatic vessels
  • lymphatic vessels:conduct flow of lymph fluid to/from lymphatic tissues/organs/cells
  • lymph: colorless water liquid made from fluid leaked from blood vessels
  • lymph carries microbes to lymph nodes, where lymphocytes & macrophages destroy pathogens
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4
Q

Whole blood contains:

A
  • plasma: water containing electrolytes, dissolved gasses, nutrients and proteins
  • RBCs: carry oxygen
  • WBCs: part of immune response
  • platelets: stop bleeding at wounds
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5
Q

Hematopoiesis

A

whole blood production

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6
Q

defensive component of blood

  • eosinophil
  • leukocytes & neutrophils
  • lymphocytes
A
  • leukocytes: defensive blood cells
  • lab tests show the type of infection
  • increased level of eosinophil: allergies or parasite
  • increased level of leukocytes & neutrophils: bacteria
  • increased level of lymphocytes: virus
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7
Q

resistance:
susceptibility:

A

resistance: ability to ward off diseases
susceptibility: lack of resistance to a disease
- humans do not have natural resistance to all pathogens

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8
Q

innate immunity

A

natural immunity: nonspecific that protects against any pathogen

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9
Q

First, second, third line of defense

A
  • first: physical barriers- skin, hair, cilia, mucus membrane, mucus & chemical secretions, digestive enzymes in mouth, and stomach acid
  • second: internal defenses- inflammatory response, complement proteins, phagocytic cells, and natural killer (NK) cells
  • third: adaptive immunity (specific resistance & uses a specialized type of cells (T&B)) - antibodies and the humoral immune system, cell-medicated immune system, and memory response
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10
Q

first line of defense

A
  • skin & mucus membrane (chemical and physical barriers)
    (chemical factors can inhibit microbial growth or destroy them)
  • human microbiome
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11
Q

skin layers & chemicals

  • antimicrobial peptides
  • perspiration
  • sebum
A
  • epidermis: multiple layers of tightly packed cells; few pathogens can penetrate from a cut; shedding of dead skin removes microorganisms; contains dendritic cells (phagocytize pathogens)
  • dermis: collagen fibers help skin resist abrasions
  • antimicrobial peptides: 20-50 amino acids secreted by dermal cells(inhibit growth of microorganisms)
  • perspiration: secreted by sweat glands. contains salt, lysosome, & dermicidins (antimicrobial proteins)
  • sebum: secreted by sebaceous glands to keep skin flexible & lowers pH
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12
Q

mucus membranes & layers

  • epithelium
  • deeper connective
A

-line all body cavities open to environment
two layers:
-epithelium: made of epithelial cells tightly packed to prevent entry of pathogens; shedding of epithelial cells carries away microbes; dendritic cells below this layer phagocytize cells; goblet & ciliated columnar cells remove invaders
-deeper connective: layer supports the epithelium

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13
Q

other physical barriers:

  • lacrimal apparatus:
  • saliva:
  • urine:
A
  • lacrimal apparatus: washes eyes with tears
  • saliva: washes microbes off teeth
  • urine: cleanses urethra and flows out
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14
Q

barrier loss

A
  • loss of immunity or absence of normal immunity
  • patients w/ severe burns, blockages in salivary glands, tear ducts, intestines, and urinary tracts
  • First LOD alone is not sufficient protection
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15
Q

normal microbiota/microbial antagonism

A

-makes it hard for pathogens to complete their normal activities
normal microbiota:
-consume nutrients
-create an unfavorable environment(pH, waste products)
-stimulate bodys 2nd LOD
-promote overall health by providing vitamins

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16
Q

antimicrobial secretions

  • gastroferritin
  • transferrin
A
  • stomach acid digests/inhibits microorganisms
  • gastroferritin (stomach) & transferrin (blood) hide/take away iron which microorganisms need
  • bile inhibits growth of most microorganisms
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17
Q

Second line of defense

A
  • when pathogens penetrate the skin or mucus membrane
  • important factors in 2nd LOD: plasma, WBCs, neutrophils & macrophages, and eosinophils
  • carries out these processes: fever, inflammation, phagocytosis, and chemical defenses (antimicrobial protiens)
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18
Q

phagocytes & two types

A

-cells that ingest/engulf microbes or particles of a cell
types:
-neutrophils: act early, recruited by inflammation, component of pus
-macrophages: present in tissues
we can distinguish they type of macrophage by its location (spleen, bone marrow, alveolar, knupffer cells, dendritic cells, brain)

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19
Q

process of phagocytosis

A
  1. chemotaxis: uses pseudopods to move towards microorganisms
  2. adherence: binding complementary chemicals on the surface of the cell wall
  3. ingestion: pseudopod fuse to form a food vesicle called, phagosome
  4. maturation: lysosome fuses w/ phagosome to form, phagolysosome which contains digestive chemical
  5. killing: the digestive chemicals have reactive forms of oxygen & acidic pH of the phagolysosome which kills the microorganisms
  6. elimination: remnants of microorganism are released by exocytoxins
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20
Q

microbial evasion of phagocytosis

A
  • capsule makes microorganisms slippery and inhibit adherence: Streptococcus pneumoniae
  • leukocidins prevent phagosome-lysosome fusion: S. arueus
  • Lyse phagocytes by membrane attack complex: Listeria mobocytogenes
  • escape phagosome: Shigella
  • survive in phagolysosome: Coxiella burnettil
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21
Q

signs of inflammation

A

-redness
-heat
-swelling
-pain
redness & heat reduced by histamine & kinin, allow for: vasodilation
swelling & pain mediated by: prostaglandin & leukotriene, when cause increased permeability

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22
Q

inflammation

A
  • destroys agents or limits their effectiveness
  • repairs or replaces damaged tissues
  • dilation caused by histamine & kinin
  • increased permeability of blood vessels is mediated by prostaglandin & leukotriene
  • neutrophils arrive first, then monocytes
  • tissue repair occurs when extra nutrients & oxygen are delivered
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23
Q

fever

A
  • body temp. at 37c
  • pyrogens/cytokines trigger hypothalamus to increase body temp. by releasing prostaglandins
  • fever is protective
  • enhance effect of interferon, inhibits growth of microbes, enhance innate or adaptive immune processes
24
Q

interferons: INFs

A

-proteins released by host cells (lymphocytes & macrophages) to inhibit viral replication and bacterial pathogens

25
Q

types of INFs

A
  • Type 1: INF-α (epithelium & leukocytes) & INF-β (tribroblasts) cause cells to produce antiviral proteins
  • Type 2:INF-γ produced by lymphocytes that causes neutrophils & macrophages to phagocytize bacteria
26
Q

complement

A

serum proteins produced by the liver, when activated, results in lysis of foreign cells

27
Q

complement activation:

A
  • opsonization: enhances phagocytosis by promoting attachment
  • cytolysis: membrane attack complex leads to cytolysis
  • inflammation: activated complement proteins bind to mass cells which release histamine to cause inflammation
28
Q

complement inactivation

A

proteins bind and break down activated complement proteins

29
Q

nonphagocytic killing

A
  • eosinophils: attach to surface of parasitic helminths and secrete toxins that weaken or kill the parasites; release mitochondrial DNA and potions that kill bacteria
  • natural killer lymphocytes: secrete toxins onto surface of cells infected w/ tumors or viruses
  • neutrophils: (inolved in phagocytosis) produce chemicals that kill nearby invaders; generate extracellular fibers that bind and kill bacteria, this is called NETs
  • neutrophil extracellular traps NETs
30
Q

nonspecific chemical defenses

A
  • trigger a response and recruit more immune system helpers
  • toll-like receptors: in membrane of phagocytic cells (host cells); bind Pathogen-Associated molecular Patterns PAMPs; when they are bound: apoptosis, secrete inflammatory mediators, stimulate adaptive immune response
  • NOD proteins: in cytosol; bind PAMPs; trigger inflammation and apoptosis, mutation in NOD genes are associated w/ immune deficiency diseases like IBS or chromes disease
31
Q

adaptive immunity

A
  • body recognizes & defends against pathogens/invaders and their products
  • lymphocytes (B & T cells) mediate these actions
32
Q
  • specific:
  • inducible:
  • clonal:
  • unresponsive to self:
  • memory:
A
  • specific: only acts against one molecular shape
  • inducible: activated when pathogen is present
  • clonal: form many generations of cells when induced
  • unresponsive to self: immune responses do not attack self
  • memory: responds more quickly to pathogens that have previously encountered
33
Q

antigens

A

portions (whole bacteria or part of a single molecule) of cells & viruses that begin the immune response

  • lymphocytes & antibodies bind to epitopes to trigger adaptive immune response
  • epitopes: binding site of an antigen
34
Q

types of antigens

  • exogenous antigens:
  • endogenous antigens:
  • autoantigens
A
  • exogenous antigens: (outside of cell wall or secreted) toxins, secretions, components of cell wall, pili, & flagella
  • endogenous antigens: protozoa, fungi, bacteria & viruses that replicate inside a cell
  • autoantigens: self-antigens from normal cellular processes
35
Q

Immunological development

A

1: lymphocyte development & clonal deletion (B & T cells mature and remove autoantigens)
2: presentation of antigens & clonal selection (B & T cells bind to antigens and replicate the selected)
3: challenge B & T cells
4: -T-lymphocyte response: cell mediated
- B-lymphocyte response: creates antibodies

36
Q

where are lymphocytes

  • b-lymphocyte
  • t-lymphocyte
A
  • lymphocytes are made by hematopoiesis from blood stem cells in bone marrow
  • B-lymphocytes: mature in bone marrow, involved in humoral immune response; activated into plasma cells which release antibodies
  • T-lymphocytes: mature in the thymus, involved in cell mediated immune response; acts against intracellular pathogens; produces cytokines which results in the elimination of pathogens
37
Q

T-lymphocyte

A
  • act against internal pathogens in cell-mediated immune response
  • make up 70-85% of lymphocytes
  • maturation in thymus & produces T cell receptor TCR to be placed on each cells cytoplasmic membrane. TCR binds to etiopope of antigen
  • antigen presenting cells: dendritic cells engulf & degrade microbes to display T cells
38
Q

cell-mediated immune response

A 
1 antigen presentation
2 helper T cell differentiation 
3 clonal expansion
4 self-stimulation 
5 -cytotoxix T cells killing (CD4): perforin-granzyme OR CD95
OR -activates B cells (CD8)
39
Q

perforin-granzyme cytotoxic pathway

A
  • perforin-granzyme: vesicles in cytoplasm of cytotoxic T cells
  • vesicles fuse w/ cytoplasmic membrane to exit T cell & enter infected cell
  • perforins create pores/channels in infected cell
  • granzyme enters channel and activates apoptosis
  • apoptosis: programed cell death
40
Q

CD95 cytotoxic pathway

A
  • present in membrane of animal cells
  • cytotoxic T cells binds to CD95 w/ receptor proteins (CD95L)
  • triggers apoptosis
41
Q

memory T cells

A
  • contacts an epitope-MHC 1; produces cytotoxic T cell clone
  • do not kill
  • if second exposure to pathogen w/ specific epitope, cell mediated immune response is more effective and quicker
42
Q

T cell regulation

A

sends signals to cytotoxic T cells to start or stop immune response

43
Q

B cell

A
  • spleen, lymph nodes, and MALT
  • small % of lymphocytes
  • function: secrete antibodies
  • each B cell has the same and several copies of BCR
  • contains 4 polypeptide chains, 2 heavy and 2 light, linked by covalent bonds between sulfur atoms
44
Q

antibodies

A
  • immunoglobulins
  • secreted by plasma cells
  • have antigen binding sites that are identical to BCR sites
45
Q

antibody binding to epitope leads to:

A
  • inflammation
  • activate complement
  • opsonization
  • direct killing
  • neutralization
  • agglutination
  • antibody dependent cytotoxicity
46
Q

classes of antibodies

  • IgM:
  • IgG:
  • IgA:
  • IgE:
  • IgD
A
  • IgM: 1st produced, pentamer, agglutinates microbes
  • IgG: most common & long lasting, 80% Ig in serum, monomer, crosses placenta (protect developing child)
  • IgA: body secretions(tears), dimer
  • IgE: response to parasitic & allergies infections, monomer
  • IgD: unknown function, monomer
47
Q

how are antibodies produced

A
  • T-independent antigens: no helper T cells needed

- T-dependent antigens: helper T cells activates the B cells

48
Q

memory b cells

A
  • made: during B cell proliferation
  • dont secrete antibodies. their BCR s identical to epitope
  • cells persist over 20 years & can initiate antibody production
49
Q

Types of adaptive immunity

A
  • naturally acquired active: you are infected; antibodies are made as a result
  • naturally acquired passive: maternal antibodies acquired
  • artificially acquired active: vaccine introduces antibodies & causes B cell activation
  • artificially acquired passive: immunotherapy where antibodies are injected (antisera or antitoxins); used when toxins and pathogens are so deadly active immune response in inadequate
50
Q
  • vaccination:

- herd immunity:

A
  • vaccination: use of antigens or antibodies to provide some immunity; (produces a primary immune response, leads to formation of antibodies and memory cells, produces a rapid and intense secondary response)
  • herd immunity: immunity in most of the population; outbreaks are sporadic due to lack of susceptible individuals
51
Q

types of artificial immunity

first vaccine

A
  • active immunization: patient mounts an immune response
  • passive immunization: patient acquires antibodies
  • Jener used Cowpox against Smallpox 1796
52
Q

attenuated vaccine

A
  • use of pathogen with reduced virulence (attenuated pathogen)
  • results in strong immune response and mild symptoms
  • may result in contact immunity
53
Q

inactivated vaccine and three types

  • whole agent:
  • subunit:
  • conjugated:
A
  • whole agent: deactivated whole microorganism (many antigens)
  • subunit: part of microorganisms (not as many antigens)
  • conjugated: proteins (strong antigens) conjugated to carbs (weak antigens)
  • booster might be required for full immunity
54
Q

toxoid vaccine

A
  • chemically or thermally modified toxins that stimulate immune response
  • require multiple doses b/c toxins contain few antigens
55
Q

recombinant gene technology

A

delete gene from pathogen producing ani irreversibly weaker microbe

  • produce large quantities of antigens
  • genetically altered bacteria or viruses may express the antigen as a vaccine
56
Q

adjuvants

A

chemicals added to vaccines to improve effectiveness

  • enhances immunogenicity
  • improve innate immuunity
  • most common in US: alumis (aluminum salt)
57
Q

vaccine Saftey

A

-safest and most effective in children
-complications:
fever, allergies, local reactions

Micro (8 decks)

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