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Molecular Immunology > Module 11 > Flashcards

Module 11 Flashcards

1
Q

extracellular bacteria cause disease by

A

inducing inflammation which results in tissue destruction at the site of infection and producing toxins such as endotoxins or exotoxins

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2
Q

the principal mechanisms of innate immunity are

A

complement activation, phagocytosis, and the inflammatory response

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3
Q

what activates the alternative complement pathway

A

LPS in the cell walls of gram negative bacteria

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4
Q

what activates the lectin complement pathway

A

mannose expressing bacteria

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5
Q

TLR and FC receptor signaling can induce what

A

the production of cytokines and acute phase proteins

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6
Q

what part of the alternative pathway binds to the microbe cell

A

c3b

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7
Q

what is the c3 convertase of the alternative pathway

A

c3bBb

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8
Q

what is the c5 convertase of the alternative pathway

A

c3bBbc3bc5

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9
Q

lectin pathway initiation

A

binding of mannose to mannose binding lectin

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10
Q

what is the c3 convertase of the lectin pathway

A

c4b2a

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11
Q

what is the c5 convertase of the lectin pathway

A

c4b2ac3bc5

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12
Q

killing of phagocytosed microbes is done by what

A

ROS and NO

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13
Q

the principal protective immune response functions to block infection, eliminate microbes, and neutralize toxins

A

humoral immunity

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14
Q

polysaccharide ig

A

igm

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15
Q

protein ig

A

iga igg

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16
Q

what are effector mechanisms

A

phagocytosis, classical complement pathway, IgM and IgG and neutrailization

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17
Q
A
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18
Q

protein antigens from extracellular bacteria can activate what

A

cd4 helper t cells

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19
Q

TH1 generates what

A

IFN-y

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20
Q

TH17 mediates what

A

responses that eliminate extracellular microbes

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21
Q

IL-17 does what

A

causes inflamation

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22
Q

IFN-y does what

A

activates macrophages to phagocytoes and kill bacteria

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23
Q

what are the consequences of host response to extracellular bacteria

A

inflammation and spetic shock

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24
Q

what causes septic shock

A

disseminated infections by gram neg bacteria

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25
Q

what is the principal mediator of septic shock

A

TNF, IFN-y and IL-12

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26
Q

viral or bacterial proteins that bind simultaneously to Vb domain of TCR and the alpha chain of class 2 MHC molecule

A

superantigens

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27
Q

exogenous

A

exotoxins

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28
Q

endogenous

A

viral proteins

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29
Q

Activation by superantigens is

A

polyclonal

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30
Q

what is polyclonal

A

superantigens bind outside the tcr antigen binding cleft and affect a large number of t cells

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31
Q

protective immunity

A

activation of peptide x specific t cell clones only

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32
Q

super antigen binding to mhc 2

A

polyclonal activation of vb3 t cells causing cytokine storm and deletion of t cells

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33
Q

what causes rhematic fever

A

pharyngeal infections with some type of beta hemolytic streptococci

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34
Q

pharyngeal infections cause

A

production of antibodies against bacterial cell wall protein m

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35
Q

m protein antibodies do what

A

cross react with myocardial proteins and deposit in the heart causing inflammation and damage

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36
Q

intracellular bacteria can do what

A

survive and replicate within phagocytes where they are inacessable to antibodeis

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37
Q

how do intracellular bacteria activate nk cells

A

they induce expression of nk activating ligands on infected cells or stimulate the production of IL-12 by DCs and macrophages

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38
Q

NK cells produce IFN-gamma which does what

A

activates macrophages

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39
Q

macrophages infected with microbes produces what which actives nk cells to produce what which stimulates macrophages to kill phagocytosed microbes

A

IL-12 IFN-y

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40
Q

how do t cells activate macrophages

A

through CD40 signaling and IFN-y

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41
Q

CD4 t cells differentiate into

42
Q

what cause the differentiation of CD4 t cells into TH1

43
Q

how can phagocytosed bacteria stimulate cd8 t cells

A

if bacterial antigens are transported into the cytosol

44
Q

the macrophage activation that occurs in response to intracellular micrboes can also cause what

A

tissue damage

45
Q

induce delayed type hypersensitivty

A

when bacteria presist for long periods within phagocytes and cause chronic antigen stimulation resulting in the formation of granulomas

46
Q

tuberculosis results from infection by what

A

intracellular pathogens

47
Q

patients that have high antibody titers but weak cell mediated immune responses mycobacteria proliferate and macrophage activation results in destructive lesions

A

lepromatous leprosy

48
Q

patients develop stron cell mediated immunity with less tissue destruction and reduced bacterial growth

A

tuberculoid leprosy

49
Q

what is the most important factor with fungal infections

A

compromised immunity

50
Q

neutrophil deficiencys can

A

cause a predisposition to fungal infections

51
Q

where can fungi live

A

extracellular tissues and within phagocytes

52
Q

what is the primary mediators of fungal infection

A

neutrophils and macrophages

53
Q

fungi causes a strong response from what

54
Q

what are important for killing of virus infected cells

A

type 1 interferons and nk cell

55
Q

what triggers ifn production in viral responce

A

recognition of viral nucleic acids by TLRs and RIG-1

56
Q

how can nk cells recognize virally infected cells

A

decreased class 1 mhc expression

57
Q

secretion of igA can do what to viral infections

A

neutralize viruses that enter through the mucosal system

58
Q

CTLs do what

A

kill cells infected by viruses

59
Q

CTLs recognize what

A

viral peptides presented by MHC 1

60
Q

Latent infections

A

viral DNA persists in host cells but virus does not replicate or kill host cells

61
Q

how can viruses evade immune cells

A

alter their antigens by surface glycoprotiens undergoing antigenic variation through point mutation or reassortment of RNA segments

62
Q

some viruses can inhibit what

A

MHC 1 associated presentation of cytosolic protein antigens

63
Q

pxviruses

A

produce molecules that bind and block the activity of cytokines and chemokines

64
Q

epstein barr

A

produces a protein similar to IL-10 that supresses immune response

65
Q

how does hiv survive

A

by infecting and eliminating CD4 t cells

66
Q

why are most parasitic infections chronic

A

weak innate immunity and the ability to evade adaptive immune responses

67
Q

parasitic infections activate what kind of immunity

68
Q

helminths are able to avoid immune responses due to

A

teguments that make them resistant to the cytocidal mechanisms of phagocytes adn develop resistance to complement mediated lysis

69
Q

what is the defense mechanism against protozoa

A

cell mediated immunity specifically the activation of macrophages by th1 cytokines

70
Q

what causes malaria

A

plasmodium

71
Q

what serves as a vector for malaria

A

female anopheles mosquito

72
Q

what cycle of plasmodium enters through mosquito bite

A

sporozites

73
Q

plasmodium sporozites in the liver transform into what

A

merozoites

74
Q

merozites infect what

A

red blood cells

75
Q

what is the difficulty with immune response to malaria

A

antibodies are only effective against a specific life stage

76
Q

CLTs can kill what kinda malaria

A

sporozoite infected hepatocytes

77
Q

how do cd8 t cells kill sporozite infected hepatocytes

A

they secrete ifn-y to activate hepatocytes to produce NO to kill parasites

78
Q

what cells mediate helminth infections

79
Q

how do th2 cells responde to helminth infections

A

production of IgE and activation of eosinophiles

80
Q

what recruits eosinophils to helminth infectiins

A

IgE and IgA

81
Q

th2 cells produce what that helps with the development of eosinophils

82
Q

how do parasites evade protective immunity

A

reducing their immunogenicity and inhibiting host immune response

83
Q

sporozite stage of malaria differ how from the merozite stage

A

antigenically

84
Q

why is it difficult to design an effective vaccine against trypanosomes

A

antigenic variation

85
Q

what stage of development must be targeted in plasmodium to prevent the infection of liver cells

A

sporozoites

86
Q

what is an innate immunity mechanism for eradicating established viral infections

87
Q

what is not a part of the innate immune response to extracellular bacteria

A

nk cell activation

88
Q

what are a part of the innate immune response to extracellular bacteria

A

complement activation by LPS and mannose, activation of phagocytes by TCR, inflmation

89
Q

what is an adaptive immunity mechanism for eradicating an established viral infection

A

CD8 t cells

90
Q

antigenic variation allows for the evasion of what type of immune recognition

A

antibody recognition of microbial surface molecules

91
Q

what is an adaptive immunity mechanism for preventing viral infection

A

antibodies which can neutralize viruses before they infect cells

92
Q

what is the main mechanism of adaptive immunity to fungi

A

cell mediated immunity

93
Q

extra cellular fungi produce a repsonse from what cells

94
Q

fungal products activate what cells

A

dendritic cells

95
Q

dendritic cells that are stimulated by fungi products produce what

A

IL-6 and IL-23

96
Q

what mediates the innate immune response to intracellular bacteria

97
Q

macrophages produce what to activate nk cells

A

IL-12 and IL-15

98
Q

TSST-1 is presented by what

A

MHC 2 to t cells that have a tcr v-beta gene segment

99
Q

TSST-1 presentation by mhc 2 causes what

A

polyclonal activation of many t cells and a large release of inflammatory cytokines

100
Q

what immune evasion strategy does influenza use

A

antigenic variation

Molecular Immunology (6 decks)

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