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Micro > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

what does the first line of defense in innate immunity consist of

A

nonspecific external barriers
- skin and mucous membranes

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2
Q

what does the second line of defense in innate immunity consist of

A

innate immune response
- phagocytic and NK cells, inflammation, and fever

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3
Q

what does the third line of defense in innate immunity consist of

A

adaptive immune response
- cell-mediated immunity and humoral immunity

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4
Q

characteristics of innate immunity
- specificity, are we born with it, does it function immediately, does it have memory, what does it recognize

A
  • nonspecific
  • we are born with it
  • functions immediately
  • no memory
  • recognizes PAMPs
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5
Q

characteristics of adaptive immunity
- specificity, what does it recognize, is it immediate, are we born with it, does it have memory

A
  • highly specific
  • recognizes antigens
  • takes time to develop
  • develops throughout light (not born with it)
  • generates memory
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6
Q

what happens when our bodies encounter a bacterium but we don’t get sick

A

first line of defense
- physical, chemical, and cellular barriers

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7
Q

how does the skin help with being in the first line of defense

A
  • the skin has tightly packed cells that don’t let microbes penetrate it
  • it is slightly acidic
  • the outermost layer sheds off
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8
Q

mucous membrane is involved in the first line of defense, what characteristics about it make it helpful

A
  • it lines the digestive, respiratory, and genitourinary tracts
  • mucus traps microbes, contains chemicals
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9
Q

what are some mechanically moving microbes

A
  • mucociliary escalator
  • peristalsis
  • lacrimal apparatus (tears)
  • saliva
  • urine and vaginal secretion
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10
Q

what does the mucociliary escalator do

A

move microbes out of respiratory tract

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11
Q

what and where is peristalsis

A

it moves the food down and along in the gut

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12
Q

what does lacrimal apparatus (tears) wash out

A

the eyes

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13
Q

what does saliva flushes out

A

the mouth

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14
Q

urine and vaginal secretions flush out the

A

genitourinary tract

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15
Q

what does normal microbiota do as a first line of defense physical barrier

A
  • compete with pathogens for cellular binding sites and available proteins
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16
Q

what does normal microbiota secrete

A

antimicrobial products and waste products that are toxic to pathogens

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17
Q

what is involved in the chemical barriers of the first line of defense in innate immunity

A
  • lysozyme
  • peroxidase
  • lactoferrin
  • salt
  • sebum
  • low pH in stomach and vagina
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18
Q

what is the function of lysozyme

A

cleaves bond between NAG and NAM in peptidoglycan

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19
Q

what does peroxidase generate

A

ROS

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20
Q

what is the function of lactoferrin

A

sequester iron that microbes need for growth

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21
Q

what does sebum seal off

A

the pore of the hair follicle

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22
Q

what does salt accumulate from

A

perspiration

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23
Q

where is there a low pH and normal microbiota

A

in the vagina

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24
Q

what are the components of the innate immune response

A
  • recognition of PAMPs
  • inflammation and phagocytosis
  • complement proteins
  • type 1 IFNs
  • NK cells
  • fever
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25
Q

what are leukocytes

A

white blood cells (WBC’s)

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26
Q

what is a lymphocyte

A

a specific type of WBC

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27
Q

what do lymphocytes recognize

A

antigens

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28
Q

what immune response do lymphocytes participate in

A

adaptive

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29
Q

what is the goal of acute inflammatory response

A

to contain, destroy, and remove pathogens and initiate the process of healing

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30
Q

how does acute inflammation work

A

moves immune cells and inflammatory proteins from the blood to the site of infection where they destroy pathogens

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31
Q

what is the goal of chronic inflammation response

A

to contain, destroy, and remove persistant pathogens

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32
Q

what happens if chronic inflammatory response fails

A

it contains the infection until the adaptive immune response fully develops which will clear the infection

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33
Q

are PAMPs shared by humans

A

no

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34
Q

how do innate immune cell recognize pathogens

A

non-specific recognition

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35
Q

true or false - pattern recognition receptor (PRR) is an example of a toll-like receptor

A

true

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36
Q

what are three toll-like receptors (TLRs)

A
  • lipopeptide
  • flagellin
  • peptidoglycan
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37
Q

mannose binding protein is another type of what

A

PRR

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38
Q

what is an opsonin

A

it is a soluble host protein
- coats the outer surface of a pathogen allowing phagocytes to bind and engulf more efficiently

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39
Q

what are the two major opsonins

A
  • C3b -> recognize PAMPs
  • IgG Ab -> recognize antigens
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40
Q

what are the eight steps to acute inflammatory response

A
  1. macrophage releases vasoactive substances and cytokines
  2. mast cell degranulates
  3. histamine releases (vasoactive)
  4. vasodilation
  5. increased permeability and edema
  6. diapedesis - PMNs traveling to site of infection
  7. chemotaxis - movement towards or away gradient - towards site of infection
  8. phagocytosis
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41
Q

true or false - C5a is also chemotactic

A

true

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42
Q

what process are TNF-alphas apart of

A

phagocyte migration

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43
Q

what are the six steps in phagocyte migration

A
  1. circulating blood
  2. endothelial cells receive signals from tissue to upregulate adhesion proteins
  3. roll along inside vessel (selections)
  4. stable adhesion (ICAM1)
  5. diapedesis (WBC squeezes out between endothelial cells of the blood vessel to go to tissue)
  6. chemotaxis
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44
Q

at the start of inflammation what is the most abundant

A

neutrophils

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45
Q

at the end of inflammation what is the most abundant

A

monocytes
- turn into macrophages when leave the blood vessel

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46
Q

when pathogen destruction is occurring by phagocytes what does the pH go down to

A

4-5

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47
Q

what happens in nonoxidative killing

A

once the phagosome fuses with the lysosome, the engulfed bacteria are degraded by lysosomal enzymes (lysozyme, phospholipase, and proteases)

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48
Q

why is it important that the fusion of phagosome and lysosome enhance acidification

A

for activation of pH-dependent lysosomal enzymes

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49
Q

what happens in oxidative killing

A

activated phagocytes undergo a respiratory burst
- increase their uptake and consumption of oxygen

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50
Q

the increased oxygen in oxidative killing is metabolized into

A

ROS
- reactive oxygen species

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51
Q

what does ROS degrade

A

bacteria

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52
Q

which cells do phagocytosis
- neutrophils
- macrophages
- dendritic cells
- all of the above

A

all of the above

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53
Q

what are cytokines

A

they are proteins secreted by WBCs that act on other cells to regulate their activity

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54
Q

true or false - cytokines can only act locally

A

false
- act locally or systemically

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55
Q

what do cytokines include

A
  • chemokines
  • IFN’s
  • TNF-alpha
  • interleukins
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56
Q

what are three pro-inflammatory cytokines

A
  • interleukins = subfamily of cytokines that are in both adaptive and innate immune responses
  • chemokines = direct migration of WBCs to a site of infection (chemotaxis)
  • TNF-alpha = stimulates production of adhesion proteins (selections) on endothelial cells
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57
Q

what are other inflammatory mediators

A
  • histamine = vasodilation and increased vascular permeability
  • prostaglandins and leukotrienes = vasodilation, pain, fever, and vascular permeability
  • C3a and C5a = chemotaxis and mast cell degranulation (anaphylatoxin)
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58
Q

what can macrophages do in chronic inflammation

A

they become activated by cytokines (which are released by Th2 cells from adaptive)
- stimulate ROS production = increased phagocytic power
- secrete large quantities of cytokines that maintain the inflammatory response

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59
Q

what do lymphocytes (T and B cells) do in chronic inflammation

A
  • major players in adaptive immune response
  • direct the attack against persistent pathogens
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60
Q

does a granuloma form everytime with chronic inflammation

A

no
- only sometimes

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61
Q

what happens if activated macrophages fail to destroy microbes

A

the macrophages will fuse together to form giant multinucleated cells

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62
Q

what three things form granulomas

A
  • giant multinucleated cells
  • macrophages
  • T cells
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63
Q

true or false - granulomas in infectious diseases may interfere with normal tissue function

A

true

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64
Q

what are granulomas called when they form in the lungs of TB patients

A

tubercles

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65
Q

what are granulomas called in syphilis

A

gummas

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66
Q

the proteins in the complement system are made where, circulate where, and enter where

A
  • made in the liver
  • circulate in the blood
  • enter the tissue
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67
Q

true or false - the serum proteins are normally inactive in the complement system

A

true

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68
Q

how are the proteins in the complement system activated

A
  • alternative pathway = C3b binding to microbial invaders
  • lectin pathway = mannose-binding lectin binding to microbial invaders
  • classical pathway (only if re-exposure) = antibodies binding to microbial invaders
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69
Q

what does C3b cause

A

opsonization

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70
Q

what does C3a + C5a cause

A

inflammation

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71
Q

what does C5b + C6-C9 cause

A

membrane attack complex (MAC) -> lysis
- create pores in membrane disrupting integrity of cell

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72
Q

how can something produced during the adaptive response activate the innate response

A

from the first exposure the body produced antibodies.
- memory of pathogen develops and antibodies are ready at re-exposure
- antibodies can easily activate classical pathway at re-exposure

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73
Q

what are the three effects of complement activation (pathways)

A
  • inflammation
  • opsonization -> enhanced phagocytosis
  • membrane attack complex -> lysis
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74
Q

what kind of toxins are C3a and C5a

A

anaphylatoxins
- bind mast cells and basophils and degranulate to release histamine (vasodilation)

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75
Q

what do C5a attract

A

phagocytes (chemotactic)

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76
Q

a patient with a genetic disorder resulting in defective complement would be most affected by a mutation in which of these?
- C1
- C3
- C5
- C9

A

C3

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77
Q

how is a fever induced

A

by pyrogens

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78
Q

what are pyrogens

A

endogenous or exogenous

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79
Q

what is the function of prostaglandins in a fever

A

they reset hypothalamic thermostate

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80
Q

do you vasoconstrict or vasodilate in fever

A

vasoconstrict because sweating and shivering

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81
Q

what are the three benefits of a fever

A
  • inhibits growth of temperature-sensitive microbes
  • speeds up phagocytosis and the repair of tissue
  • increased leukocyte motility
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82
Q

would complement proteins and phagocytosis be effective in fighting off pathogens that replicate inside cells such as viruses?

A

no

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83
Q

IFN-alpha and beta are apart of which immune response

A

innate

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84
Q

IFN-gamma is apart of which immune repsonse

A

adaptive

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85
Q

how are IFN-alpha and beta produced

A

by virally-infected cells

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86
Q

what do IFN-alpha and beta cause

A

neighbor cells to produce antiviral proteins - inhibit viral replication

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87
Q

how are IFN-gamma produced

A

by lymphocytes

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88
Q

what does IFN-gamma induce

A

neutrophils and macrophages to phagocytize bacteria

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89
Q

are NK cells innate or adaptive

A

innate

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90
Q

true or false - NK cells are a type of lymphocyte

A

true

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91
Q

true or false - NK cells kill virally

A

true

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92
Q

how do NK cells differ from T-cells

A

in the way they recognize their target

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93
Q

what are the two major immune responses

A

innate and adaptive

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94
Q

what are the two branches of the adaptive immune response

A
  • cell-mediated immunity
  • humoral immunity
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95
Q

what are the subcategories of cell-mediated immunity

A
  • cytotoxic T-lymphocytes
  • activated macrophages
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96
Q

what are the subcategories of humoral immunity

A
  • B lymphocytes
  • antibody proteins
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97
Q

is cell-mediated immunity intracellular or extracellular

A

intracellular

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98
Q

is humoral immunity intracellular or extracellular

A

extracellular

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99
Q

in cell-mediated immunity what do lymphocytes act against

A

target cell

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100
Q

describe how lymphocytes in cell-mediated immunity directly act against target cells

A

by killing infected cells

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101
Q

how to lymphocytes in cell-mediated immunity act indirectly against target cells

A

by releasing chemicals that enhance inflammatory response
- or by activating other lymphocytes or macrophages

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102
Q

in humoral immunity where are the antibodies circulating

A

freely in body fluids

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103
Q

what do B cells activate

A

antibodies

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104
Q

in humoral immunity do the antibodies bind permanently or temporarily to the target cell

A

temporarily

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105
Q

what happens in humoral immunity when the antibody temporarily binds to the target cell

A
  • temporarily inactivate
  • mark for destruction by phagocytes or complement
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106
Q

what are the two types of response in adaptive immunological memory

A
  • primary response = occurs after initial contact with Ag
  • secondary response = occurs after subsequent exposures
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107
Q

B cells differentiate into

A

plasma cells and memory cells

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108
Q

T cells differentiate into

A

helper T cells, cytotoxic T cells, and memory cells

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109
Q

does BCR recognize whole antigen or parts of antigen

A

whole antigen

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110
Q

does TCR recognize whole antigen or parts of antigen

A

parts of antigen

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111
Q

where do B cells and T cells develop

A

bone marrow

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112
Q

where do B cells mature

A

bone marrow

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113
Q

where do T cells mature

A

thymus

114
Q

what are the primary lymphoid organs

A

thymus and bone marrow

115
Q

what are the secondary lymphoid organs/tissues

A
  • lymph nodes
  • spleen
  • clusters of lymphoid tissue in gut (GALT) and tonsils and breast (MALT)
116
Q

____ but still ___ lymphocytes leave the thymus and bone marrow

A

immunocompetent and naive

117
Q

___ cells and effector ___ cells circulate continuously in the blood and lymph and throughout the secondary lymphoid organs

A

memory and T

118
Q

what are naïve lymphocytes

A

they are lymphocytes that have antigen receptors, but have not yet encountered their specific antigen

119
Q

what are activated lymphocytes

A

they are lymphocytes that have bound antigen to their antigen receptor and have received a co-stimulatory signal
- they are able to expand and differentiate into effector and memory cells

120
Q

what are effector lymphocytes

A

they are short-lived descendants of activated lymphocytes
- can carry out specific immune functions

121
Q

what are memory lymphocytes

A

long-lived descendants of activated lymphocytes
- can quickly become active effector lymphocytes on second exposure to antigen

122
Q

what is an antigen

A

a foreign substance recognized by a BCR, TCR, or antibody (Ab)

123
Q

true or false - each microbe or noninfectious foreign substance has the same antigen

A

false
- antigens are unique to each one (like a name tag)

124
Q

how did antigen get its name

A

antibody generator

125
Q

what can be antigens

A
  • proteins
  • polysaccharides
  • conjugates of lipids with proteins and polysaccharides
126
Q

what is immunogenicity

A

has the ability to induce humoral and/or cell-mediated immune response

127
Q

what is an immunogen

A

a substance that induces response

128
Q

what is antigenicity

A

has the ability to combine specifically with Abs or TCR/MHC or BCR but may or may not induce an immune response

129
Q

true or false - not all antigens are immunogenic

A

true

130
Q

what are haptens

A

they are too small to induce a response
- lack immunogenicity

131
Q

if hapten is coupled to a carrier protein is it able to induce an immune reponse

A

yes

132
Q

what are epitopes apart of

A

antigens

133
Q

what can recognize an epitope

A
  • BCR
  • TCR
  • antibody (Ab)
134
Q

true or false - a typical protein only has one unique epitope

A

false
- a typical protein has multiple epitopes

135
Q

predict which of the following is the most immunogenic (ie which elicits the strongest immune response)
- ss DNA
- self (host) protein
- piece of plastic
- bacterial cell
- bacterial pilus protein

A

bacterial cell

136
Q

what makes a good antigen

A
  • large size (more epitopes)
  • complexity/heterogeneity
  • proteins generally elicit strong response
137
Q

what are the two that elicit weak responses

A
  • polymers
  • lipids are haptens
138
Q

how many antigen-binding sites do the BCR’s recognize

A

two

139
Q

how many antigen-binding sites do TCR’s recognize

A

one

140
Q

what kind of antigens do BCR bind to

A

free soluble antigens

141
Q

what kind of antigens do TCR bind to

A

binds processed antigens that are presented to them by MHC receptor
- don’t bind soluble antigen

142
Q

true or false - each B and each T cell express a unique BCR or TCR that recognizes one single epitope

A

true

143
Q

can B or T cells bind to identical antigens

A

yes

144
Q

do BCRs and TCRs vary from cell to cell

A

yes

145
Q

genetic rearrangement in T cell: what makes up the alpha chain

A

one V-alpha segment and one J-alpha segment

146
Q

genetic rearrangement in T cell: what makes up the beta chain

A

one V-beta segment, one D-beta segment, and one J-beta segment

147
Q

all of the genetic rearranging in the T cell provide

A

genetic diversity

148
Q

for negative selection of autoimmune clones, lymphocytes that react with self antigens (autoimmune) undergo apoptosis (negative selection) in

A

bone marrow (B cells) or in thymus (T cells)

149
Q

what is the purpose of lymphocytes in negative selection to undergo apoptosis

A

prevents self-reacting T and B cells from reaching the bloodstream and potentially causing autoimmune disease

150
Q

what do activated CD4+ T cells differentiate into

A

helper T cells and memory cells

151
Q

what are the two types of helper T cells

A

Th1 and Th2

152
Q

why do helper T cells secrete cytokines

A

to activate other cells of the immune response

153
Q

what does IL-2 activate

A

CD8+ T cells

154
Q

what does IFN-gamma activate

A

macrophages

155
Q

what does IL-4,5 activate

A

B cells

156
Q

what does CTL mean

A

cytotoxic T cell

157
Q

what do activated CD8+ T cells differentiate to

A

cytotoxic T cells and memory cells

158
Q

CTL bind ___, make ___, and kill

A

bind cells, make holes (perforin) and kill (granzymes)

159
Q

what are CTL effective against

A

intracellular pathogens particularly viruses

160
Q

true or false - T cells only recognize short fragments of antigens (peptides of about 8-25 aa’s)

A

true

161
Q

what are APCs

A

professional antigen presenting cells

162
Q

what are APCs

A

they are specialized cells that internalize antigen by phagocytosis or endocytosis and then express parts of the antigen on their cell surface via MHC receptors

163
Q

APCs are distinguished by what two properties:

A
  1. express MHC 2 receptors
  2. provide co-stimulatory signals necessary for activation of T cells
164
Q

what are the three kinds of APCs

A
  • macrophages
  • dendritic cells
  • B cells
165
Q

what do dendritic cells do

A

phagocytize pathogens
- most effective antigen presenter known
- strongest initiator of T cell activation
- key link between innate and adaptive immunity

166
Q

where are macrophages located

A

they are widespread in lymphoid organs and connective tissues

167
Q

what do macrophages in APCs present

A

they present antigens to T cells to activate themselves into mean phagocytes that secrete bactericidal chemicals

168
Q

what is the function of B cells in APCs

A
  • do not activate naive T cells
  • present antigens to helper T cell to assist own activation
169
Q

what are the two types of MHC receptors

A
  • MHC 1 present to CD8+ T cells -> cytotoxic T cells
  • MHC 2 present to CD4+ T cells -> helper T cell
170
Q

where are MHC 1 receptor found

A

on all nucleated cells (not RBC)

171
Q

with MHC 1 receptor how is the degradation of cytosolic proteins done

A

by proteasome

172
Q

do MHC 1 receptors present endogenous or exogenous antigens

A

endogenous

173
Q

what cells to the MHC 1 receptor present the processed antigen to

A

CD8+ T cells

174
Q

MHC 2 receptors are found on

A

professional antigen presenting cells
- APCs also express MHC 1 receptors

175
Q

how are the peptides generated in MHC 2

A

by lysosomal enzymes

176
Q

true or false - antigens presented on MHC 2 receptors are exogenous (most bacteria, toxins, and fungi)

A

true

177
Q

what cells do MHC 2 receptors present the peptides to

A

CD4+ T cells

178
Q

which type of molecule is responsible for presenting an exogenous antigen on the surface of the appropriate cell?
- TCR
- MHC 1
- MHC 2
- CD4
- CD8

A

CD4

179
Q

where in the body do APCs go to present endogenous antigens to CD8+ T cells?
- lymph nodes
- thymus
- liver
- bone marrow

A

lymph nodes

180
Q

samantha johnson has bare lymphocyte syndrome due to a lack of MHC 1 expression. this disease would be expected to result in an inability of APCs to….
- present endogenous antigen to T cells
- bind to any T cells in the lymph node
- activate any CD4 T cells
- A and C are correct
- A and B are correct

A

present endogenous antigen to T cells

181
Q

what are the two major phases of primary T and B cell response

A
  1. selection and activation of naïve lymphocytes
  2. execution of the effector function
182
Q

what happens in clonal selection

A

upon entry into immune system, each antigen is recognized by a genetically distinct lymphocyte with the “right” receptor

183
Q

what happens in clonal activation

A

signals from another cell are usually needed

184
Q

what happens in clonal expansion

A

upon activation, the lymphocyte proliferates and differentiate into a larger population of identical cells (ie clones) that can react to that antigen

185
Q

what are the three steps in activating CD4+ T cells

A
  1. requires interaction between TCR and the peptide presented on MHC 2 on the APC
  2. requires a co-stimulatory signal (B7-CD28)
  3. CD4+ T cells up-regulates IL2R and produces IL-2 to expand and differentiate into effector and memory T cells
186
Q

what do Th1 cells differentiate into

A
  • IFN-gamma -> macrophages
  • Il-2 -> CD8+ T cells
187
Q

what do Th2 cells differentiate into

A

IL-4,5 -> B cells

188
Q

with activated macrophages phagosome will be more ____ fused to the lysosomes

A

efficiently

189
Q

in activated macrophages, what are the three highly reactive and microbicidal molecules

A
  • oxygen radicals
  • nitric oxide
  • proteases
190
Q

activated macrophages are a good defense against what

A

intracellular bacteria
- eg: mycobacterium tuberculosis

191
Q

which type of lymphocytes is responsible for virus-infected host cells?
- B lymphocyte
- helper T cell
- cytotoxic T cell
- plasma cell

A

cytotoxic T cell

192
Q

what are the four steps in the activation of CD8+ T cells

A
  1. requires the interaction between TCR and peptide presented on MHC 1 on the APC
  2. requires a co-stimulatory signal from B7-CD28
  3. requires IL-2 from Th1 cell
  4. CD8+ T cell up-regulates IL2R and produces IL2 to expand and differentiate into effector and memory T cells
193
Q

can B cells recognize antigen directly

A

yes

194
Q

when B cells are activated what do they differentiate into

A

plasma cells

195
Q

what do plasma cells make and secrete

A

antibodies (Ig)

196
Q

when antigens activate B cells, they clone, and give rise to __ cells and __ cells

A

plasma and memory

197
Q

what are the two mechanisms of B cell activation

A
  1. B cell receptor bind to antigen
    - endocytose (engulf) the antigen, process it, and present on MHC 2 to Th2 cells
    - Th2 cells release IL-4,5 -> strong activation = T dependent
  2. co-stimulatory signal
    - some antigens crosslink BCR -> weak activation = T-independent
198
Q

true or false - T independent antigens are rare and highly repetitive molecules

A

true

199
Q

do T-independent B cells produce memory cells or class switch

A

no

200
Q

in T-independent B cell activation - B cells are weakly stimulated to make what class of antibodies

A

IgM

201
Q

children don’t activate ___ cells independently of ___ cells

A

B and T

202
Q

T-dependent B cells present their antigen on their MHC ___ to __ cell

A

2 and Th2

203
Q

in T-dependent B cell activation - Th2 cell produces cytokines that strongly activate the __ cell

A

B

204
Q

in T-dependent B cell activation - can B cells undergo class switching to make antibodies other than IgM

A

yes

205
Q

what are most antigens, T-dependent or T-independent

A

T-dependent

206
Q

a patient infected with HIV becomes severely immunocompromised. This is because HIV infects and destroys CD4+ T cells. Low CD4+ T cell count would result in an inability to fight off infections by which of the following?
- RNA viruses
- extracellular bacteria
- intracellular bacteria
- fungi
- all of the above

A

all of the above

207
Q

can an organism be wholly intracellular at all times

A

no

208
Q

transmission must occur between what kind of cells

A

the host’s cells

209
Q

what does the extracellular phase in the development of the pathogen provide

A

an opportunity to control infection through defense mechanisms
- phagocytosis, presentation on MHC 2, Ab, and complement

210
Q

can an APC engulf “dead” parts of viruses

A

yes

211
Q

antibodies are especially effective against ___ pathogens

A

extracellular
- eg bacteria

212
Q

what is the structure of an immunoglobulin

A
  • Ab’s are heterodimers
  • 2 identical light chains and heavy chains
  • disulfide bonds join heavy, light chains, and Fc segment
213
Q

on the immunoglobulin structure how many Fab’s and Fc’s are there

A

two Fab’s and one Fc

214
Q

the Fc on the immunoglobin structure binds to what kind of cell

A

host cell

215
Q

true or false - each antibody recognizes any general antigen

A

false
- each antibody recognizes a specific antigen

216
Q

the BCR heavy chain is made up of what segments

A

V, D, and J

217
Q

the BCR light chain is made up of what segments

A

V and J

218
Q

what do antibodies do

A

they circulate through the blood and lymph
- only interacts with specific target antigen

219
Q

what happens when Ab find its antigenic match

A

it binds to the antigen and initiates several events that destroy the targets

220
Q

what are four antibody functions

A
  1. agglutination = crosslink antigen to reduce number of infectious units to be dealt with (each side of Y attaches to a bacteria)
  2. fixes and activates complement = the stick of the Y (Ab) attaches to complement and then causes inflammation and cell lysis
  3. opsonization = enhances phagocytosis
  4. neutralization = blocks adhesion of bacteria and viruses to mucosa (also blocks attachment of toxin) - the Abs will bind to every binding spot on the bacteria, virus, and toxin so that they have no where to bind onto our mucosa
221
Q

what are the five different heavy chain constant regions

A

IgM,IgG, IgA, IgD, and IgE

222
Q

amino acid sequence in the constant region of the ___ chain determines Ig class

A

heavy chain

223
Q

IgM serves as an ___ receptor on B cells

A

antigen

224
Q

what Ab class is first produced in primary response

A

IgM

225
Q

what does IgM activate

A

complement

226
Q

why is IgM good at agglutination

A

because it has 10 antigen binding sites
- 5 antibodies

227
Q

what does the M stand for in IgM

A

multi/mega

228
Q

what does the G stand for in IgG

A

generic/general

229
Q

what Ab is the most abundant in serum

A

IgG

230
Q

which Ab is the only one that can cross the placenta

A

IgG

231
Q

what can IgG do

A
  • opsonization
  • activate complement
  • neutralize toxins and viruses
232
Q

what does IgA protect, what does it exist as, and what secretions is it in

A
  • protects mucosal surfaces
  • exists as a dimer
  • is in breastmilk, mucus, tears, and saliva
233
Q

what does IgD function as

A

a BCR

234
Q

what can IgE do

A

lysis of parasitic worms and allergic reactions

235
Q

upon first exposure which Ab is first made

A

IgM

236
Q

what does IgM change into by default

A

IgG

237
Q

in other situations, what can IgM class switch to

A

IgE or IgA

238
Q

what does class switching not alter

A

the antigen specificity

239
Q

are NK cells innate or adaptive, what kind of cells do they kill, their mechanism of killing is similar to what other cell

A
  • innate cells
  • kill infected host cells (intracellular)
  • similar mechanism of killing as CTL (make pores, induce apoptosis -> perforin, granzyme)
240
Q

immunological memory has two different responses, what are they

A

primary and secondary

241
Q

what happens in the primary immune reponse

A
  • cell proliferation and differentiation upon first antigen exposure
  • lag period: 4-7 days or longer
  • peak levels of plasma Ab are reached in 10 days
  • Ab levels then decline
242
Q

what happens in secondary immune response

A
  • re-exposure to same antigen gives faster, more prolonged, more effective response
  • sensitized memory cells respond within hours
  • Ab levels peak in 3-5 days at much higher levels
  • Ab’s bind with greater affinity
  • Ab level can remain high for weeks to months
  • pathogens usually eliminated before causing harm
243
Q

what Ab is the Ab of memory

A

IgG

244
Q

when there is a second exposure, does IgM need to be made first and then change to IgG

A

no
- can produce IgG Ab without having to first make IgM and then class switch

245
Q

what does immunization mean

A

exposure to antigen

246
Q

what does immunodiagnosis use

A

antibody-antigen interactions to identify pathogens and diagnose infection

247
Q

what is a serological test

A

in vitro diagnostic test of serum

248
Q

what is serum

A

plasma with all clotting factors removed
- the blood fraction that contains antibodies

249
Q

what is the percent of plasma, WBCS and platelets, and RBCs in immunodiagnosis

A
  • 55% plasma
  • 1% WBCs and platelets
  • 44% RBCs
250
Q

what do serological tests identify

A

antibodies

251
Q

what do immunological tests identify

A

antigen

252
Q

a positive Ab-Agn interaction is usually evident as some visible sign such as ___ ___ or ___

A

color change; clumping

253
Q

what occurs with latex agglutination test to detect Ab

A
  • latex beads coated with an antigen
  • agglutinate when mixed with patient serum if they have IgM Abs against the antigen
  • agglutinated complexes settle out and form visible clumps
254
Q

in the latex agglutination test, the agglutinated particles will be spread throughout the test tube or mostly concentrated at the bottom with the most positive reaction

A

at the bottom

255
Q

what happens with latex agglutination test to detect antigen

A
  • latex beads coated with Abs
  • agglutinate when mixed with patient serum if serum contains antigens specific to the antibodies
256
Q

why are labeled Ab tests used

A

to detect either antigens or Abs

257
Q

what are two examples of labeled Ab tests

A
  1. fluorescent Ab tests (immunofluorescence)
  2. ELISA
258
Q

what is the indicator for ELISA

A

the enzyme linked to Ab
- product has color

259
Q

how does ELISA detect Abs

A
  • a patient’s serum is added to wells in 96-well plate that has a known antigen
  • patient’s Abs bind to antigen
  • patient’s Abs are detected by a secondary Ab that is labeled with an enzyme
  • when substrate is added, the enzyme-antibody complex hydrolyzes the substrate, which releases a dye
  • wells that develop color are positive for the Ab
  • colorless wells are negative
260
Q

what does indirect ELISA detect

A

antibodies

261
Q

what does direct ELISA detect

A

antigens

262
Q

true or false - classifying adaptive immunity has active and passive immunity

A

true

263
Q

how is active immunity acquired

A

through direct stimulation of the immune system by an antigen
- produces Abs
- takes time to develop
- develops memory, lasting

264
Q

how is passive immunity acquired

A

indirectly by the donation of performed Abs produced by another human or animal
- protection without prior experience
- acts immediately
- does NOT create memory, short term

265
Q

what is an example of natural acquired and artificial acquired passive immunity

A
  • natural = breastmilk
  • artificial = blood donation
266
Q

what is an example of natural acquired and artificial acquired active immunity

A
  • natural = getting the illness itself
  • artificial = through vaccine
267
Q

what are specific types of immunotherapy

A
  • convalescent serum = serum from donor(s) who has a known exposure to a specific pathogen
  • synthetic monoclonal Abs = Abs produced in the lab-specific to an antigen on a pathogen
  • antitoxin = an Ab that recognizes and binds to a bacterial exotoxin or toxin in snake venom
268
Q

what is immunotherapy used for

A
  • patients at risk for rapidly fatal diseases
  • patients at risk for bacterial diseases involving exotoxin (ie botulism and tetanus)
  • patients who are immunodeficient (ie HIV patients and chemo patients)
269
Q

true or false - immunotherapy is part of artificially acquired passive immunity

A

true

270
Q

what does a vaccination do

A
  • deliberately expose a person to material that is antigenic but not pathogenic
  • stimulate a primary adaptive response to prepare the immune system for future exposure to a virulent pathogen (ie generate memory cells)
  • response to exposure to the virulent pathogen will be immediate and powerful due to the secondary response
271
Q

what does a vaccine contain

A

dead or weakened or subunits (parts) of pathogens that stimulates your immune system to produce Abs or CTL’s, exactly like it would if you were exposed to the disease

272
Q

true or false - vaccines = pathogen imposters

A

true

273
Q

how is herd immunity achieved

A

when critical portion of population is immune to disease

274
Q

herd immunity - the higher the immunization rate in a population, the less likely an ___ agent can spread due to insufficient susceptible hosts

A

infectious

275
Q

what does herd immunity confer

A

indirect protection for those who can’t become immune

276
Q

what is herd immunity responsible for

A

dramatic declines in childhood diseases and for prevention of epidemics

277
Q

who is unable to be immunized

A
  • immunocompromised (AIDS patients, patients taking immunosuppressive drugs)
  • pregnant women (risk to fetus)
  • elderly or babies
278
Q

one measure of contagiousness is ___

A

R0

279
Q

what does R0 represent

A

the number of people on average that an infected individual spreads an infection to

280
Q

what is the herd immunity threshold equation

A

(R0 - 1) / (R0)

281
Q

why do we still vaccinate against uncommon disease

A

to maintain herd immunity

Micro (8 decks)

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