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Immunology > Innate Immunity (part 2) > Flashcards

Innate Immunity (part 2) Flashcards

1
Q

complement system

A

consists of several plasma proteins that work together to opsonize microbes, to promote the recruitment of phagocytes to the site of infection, and in some cases, to directly kill the microbes

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2
Q

3 complement pathways

A

alternative (spontaneous) pathway

classical pathway

lectin pathway

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3
Q

complement pathway early/late steps

A
  1. formation of C3 convertase complexes that cleave C3 –> C3a (inflammation) and C3b (osponization and phagocytosis of microbes)
  2. formation of C5 convertase complexes that cleaves C5 –> C5a (inflammation) and C5b (initiates late steps - membrane attack complex)
  3. late steps results in formation of the membrane attack complexes which form holes in microbial membranes
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4
Q

complement activation involves proteolytic cascades in which an inactive precursor enzyme, called a ______ , is altered to become an active _____ that cleaves the next complement protein in the cascade

A

zymogen

protease

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5
Q

enzymatic cascades result in tremendous ______ of the amount of proteolytic byproducts that are generated

A

amplification

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6
Q

byproducts of complement activation perform various ______ functions of the complement system

A

effector

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7
Q

the complement system works in cooperation with other medically important proteolytic cascades including:

A

the blood in coagulation pathways

the kinin-kallikrein system that regulates vascular permeability

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8
Q

recognition of microbes by any of the 3 complement pathways results in a sequential recruitment and assembly of additional complement proteins into _____ complexes

A

protease

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9
Q

C3 convertase cleaves C3 producing

A

C3a and C3b fragments

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10
Q

soluble C3a fragments stimulates ______ by acting as a _______ for ______

A

inflammation

chemoattractant

neutrophils

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11
Q

C3b fragment becomes covalently attached to _____ and serves as an opsonin to promote ______ of the microbes

A

microbial surface

phagocytosis

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12
Q

C3 convertase binds to ______ to form a protease complex called ______

A

C3b

C5 convertase

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13
Q

C5 convertase cleaves C5 producing _____ and _____

A

C5a and C5b

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14
Q

soluble C5a is a very potent chemoattractant that also induces changes in

A

the permeability of blood vessels

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15
Q

C5b is attached to bacterial membrane that initiates the formation of a complex of ______ called the ______

A

C6, C7, C8, C9 complement proteins

membrane attack complex (MAC)

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16
Q

multiples MACs cause

A

bacterial leak and lysis

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17
Q

alternative pathway steps

A
  1. C3 spontaneously cleaves and C3b attaches to pathogen surface
  2. Factor B binds to C3b –> Factor D cleaves Factor B –> producing Ba and Bb
  3. C3b and Bb complex is now alternative C3 convertase (C3bBb) which can cleave more C3 molecules generating more C3a and C3b
  4. properdin binds and stabilizes the formed C3bBb convertase that enhances successive proteolytic steps producing more C3b proteins attaching to pathogen surface
  5. another C3b binds to properdin-C3bBb complex forming alternative C5 convertase (C3b2Bb)
  6. alternative C5 convertase (C3b2Bb) cleaves C5 producing C5a and C5b and C5b (along with C6 and C7) intercalates into pathogen membrane surface
  7. C5b is responsible for MAC formation
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18
Q

the alternative pathway can be initiated as an _______ when C3b generated by the classical or lectin pathway binds to microbial surface and interacts with factor B producing C3 convertases of the alternative pathway

A

amplification loop

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19
Q

Formation of MAC and lysis of bacteria

A
  1. C5b binds C6 and C7 and intercalates pathogen membrane
  2. C8 binds to the C5b67 complex
  3. C9 binds to the C5b678 complex and polymerize
  4. 1-16 molecules of C9 bind to form a pore in the membrane
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20
Q

classical pathway steps

A
  1. antibody binds to pathogen surface changing conformation of antibody
  2. C1q binds to Fc portion of antibody
  3. C1r activates C1s serine proteases
  4. C1s activates C2 and C4 producing C2aC4b complex (classical C3 convertase)
  5. classical C3 convertase (C4bC2a) cleaves C3 into C3a and C3b (C3b attaches to pathogen surface)
  6. C3b binds to C4bC2a forming classical C5 convertase (C4bC2aC3b)
  7. classical C5 convertase cleaves C5 into C5a and C5b
  8. C5b initiates formation of MAC
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21
Q

lectin pathway steps

A
  1. mannose binding lectin (MBL) recognizes terminal mannose residues on microbial glycoproteins and glycolipids (similar to the mannose receptor on phagocytes) and binds to pathogen surface activating MASP-1 and MASP-2
  2. MASP-1 and MASP-2 cleaves C4 to C4a and C4b and C2 to C2a and C2b
  3. C4b binds covalently to microbial surface
  4. C2a binds to C4b (lectin pathway convertase)
  5. C4b2a (lectin pathway convertase) binds C3 and cleaves into C3a and C3b (C3b remains binded to C3b2a)
  6. C4b2a3b (lectin pathway C5 convertase)
  7. lectin pathway C5 convertase (C4b2a3b) cleaves C5 into C5a and C5b
  8. C5b initiates formation of MAC
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22
Q

classical complement pathway:

C3 convertase

C5 convertase

A

C3: C4bC2a

C5: C4bC2aC3b

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23
Q

lectin complement pathway

C3 convertase

C5 convertase

A

C3: C4bC2a

C5: C4bC2aC3b

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24
Q

alternative complement pathway

C3 convertase

C5 convertase

A

C3: C3bBb

C5: C3bBbC3b

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25
Q

classical pathway requires

A

IgM or IgG

CI

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26
Q

in alternative pathway, C3 undergoes ______ hydrolysis

A

spontaneous

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27
Q

alternative pathways requries

A

Factors B and D

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28
Q

complement is not activated on the surface of mammalian cells because they express ______ that inhibit, disassemble, or cleave the convertases

A

complement regulatory proteins

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29
Q

DAF complement regulatory proteins

A

blocks C4b and C2a

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30
Q

DAF or CR1

A

dissociate C3 convertase (C4bC2a)

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31
Q

CR1 and Factor I

A

C3b/C4b inactivator

Factor I cleaves C4b/C3b preventing the assembly of the C3 and C5 convertase

(CR1 is cofactor for Factor I)

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32
Q

complement pathways produce soluble C3a and C5a which act as recruiters and activation of ______ resulting in _______

A

leukocytes

inflammation

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33
Q

bound C3b to pathogen surface results in

A

recognition of bound C3b by phagocyte resulting in phagocytosis

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34
Q

C3a and C5a stimulate mast cells and basophils to secrete ______ resulting in ______

A

vasoactive substances

inflammation

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35
Q

C3a and C5a stimulate neutrophils to secrete _____ resulting in _____

A

chemokines, prostaglandins, ROS, and RNS

inflammation

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36
Q

C3a and C5a stimulate monocyte and macrophage to secrete _____ resulting in _____

A

IL-1, IL-6, prostaglandins, ROS, RNS

inflammation

37
Q

there are no receptors for

A

C4a

38
Q

which is more potent stimulator of inflammation, C3a or C5a

A

C5a

39
Q

how does C3a and C5a result in inflammation

A

contraction of smooth muscles

increases permeability of blood vessels

degranulation of basophils

chemotaxis, release of O2 radicals and lysosomal enzymes

40
Q

complement-mediated phagocytosis and killing steps

A
  1. complement activation leads to deposition of C3b on the bacterial cell surface
  2. CR1 (complementary receptor 1) on macrophage binds to C3b on bacterium
  3. endocytosis of the bacterium by the macrophage
  4. macrophage membrane fuse creating a membrane-bounded vesicle called a phagosome
  5. lysosomes fuse with the phagosomes forming the phagolysosome and killing by ROS, RNS, NO, and lysosomal enzymes
41
Q

some bacteria can survive in phagolysosome because they express

A

catalase

42
Q

microbes may be ingested by different membrane receptors of

A

phagocytes

43
Q

collectins and ficolins are enhancers of

A

phagocytosis

44
Q

collectins are a family of soluble _____ with lectin head which serve as effector molecules of the innate immune system

A

PRRs

45
Q

mannose binding lectin (MBL) and pulmonary surfactant proteins ____ are members of the collectins family

A

SP-A and SP-D

Surfactant Protein (SP)

46
Q

MBL is a soluble PRR that binds to carbohydrates with terminal _____ and enhance phagocytosis of microbes

A

mannose

47
Q

low MBL levels are associated with increased susceptibility to a variety of

A

infections

48
Q

SP-A (surfactant protein A) and SP-D have ______ properties and their major functions are to maintain the ability of lungs to expand and as mediators of innate immune responses

A

lipophilic

49
Q

SP-A and SP-D bind to various microorganisms and act as _____ , facilitating phagocytosis by ______ macrophages

A

opsonins

alveolar

50
Q

SP-A and SP-D can also directly inhibit ______ growth and directly activate______

A

bacterial

macrophages

51
Q

ficolins are a family of

A

PRRs

52
Q

ficolins are plasma proteins (humoral molecules) that are structurally similar to collectins but they have a fibrinogen-type ______ recognition domains

A

carbohydrate

53
Q

ficolins recognize ______ and ______ on the surface of microbes and activates _____ complement pathway through activation of MASP1 and MASP2

A

N-acetylglucosamine

lipoteichoic acid

lectin

54
Q

ficolins limit ongoing ______ growth

A

bacterial

55
Q

collectins and ficolins are ______ molecules (PRRs) which recognize pathogen surface proteins

A

humoral

56
Q

C1q binds to the Fc regions of _____ and activates _____ and _____ which initiates ______ complement pathway

A

IgM

C1r

C1s

classical

57
Q

MBL (collectin) binds _____ on the surface of pathogens and activates _____ complement pathway by activation of MASP1 and MASP2

A

mannose

lectin

58
Q

cytokine: Tumor Necrosis Factor (TNF)

produced by:

cellular target and effect:

A

macrophages* ; T-cells

endothelial cells: activation (inflammation, coagulation)***

neutrophils: activation
hypothalamus: fever
liver: synthesis of acute-phase proteins

muscle, fat: catabolism

many cell types: apoptosis

59
Q

cytokine: IL-1

produced by:

cellular target and effect:

A

macrophages** ; DCs, endothelial cells, T cells, fibroblasts, platelets

endothelial cells: activation (inflammation and coagulatioon)

hypothalamus: fever***
liver: synthesis of acute phase proteins

60
Q

cytokine: chemokines

produced by:

cellular target and effect:

A

macrophage*** ; DCs, endothelial cells, T cells, fibroblasts, platelets

leukocytes: increased integrin affinity, chemotaxis, activation

61
Q

cytokine: IL-12

produced by:

cellular target and effect:

A

macrophages*** ; DCs

NK cells and T cells: IFN-gamma production

62
Q

cytokine: IFN-gamma

produced by:

cellular target and effect:

A

NK cells and T cells

activation of macrophages –> production of cytokines

63
Q

cytokine: Type 1 IFNs (alpha and beta)

produced by:

cellular target and effect:

A

IFN-a: macrophages*** ; DCs
IFN-b: fibroblasts

all cells: antiviral***, increased class I MHC expression

NK cells: activation

64
Q

cytokine: IL-10

produced by:

cellular target and effect:

A

macrophages*** ; DCs, T cells

macrophages, DCs: inhibition of IL-12 production, reduced expression of costimulators and class II MHC molecules

65
Q

cytokine: IL-6

produced by:

cellular target and effect:

A

macrophages*** ; endothelial cells, T cells

liver: synthesis of acute-phase proteins***

B cells: proliferation of plasma cells

66
Q

cytokine: IL-15

produced by:

cellular target and effect:

A

macrophages***

NK cells: proliferation

T cells: proliferation

67
Q

cytokine: IL-18

produced by:

cellular target and effect:

A

macrophages

NK cells and T cells: IFN-gamma synthesis***

68
Q

cytokine: TGF-beta (transforming growth factor)

produced by:

cellular target and effect:

A

macrophages and many others

inhibition of inflammation

69
Q

first sign of systemic inflammatory response is

A

fever

70
Q

sickness cytokine (what makes you feel miserable)

A

TNF

71
Q

TNF and IL-1 act locally on leukocytes and endothelium to induce acute _______ and induce expression of cytokine ______

A

inflammation

IL-6

72
Q

TNF, IL-1, and IL-6 mediate protective systemic effects of inflammation, by inducing ______, _______ synthesis by the liver, and _______

A

fever

acute-phase protein

leukoctyosis (increased production of leukocytes by the bone marrow )

73
Q

systemic TNF can cause the pathologic abnormalities that lead to septic shock, including:

decreased ______ function

thrombosis and ______ leak

metabolic abnormalities due to ______ resistance

A

cardiac

capillary

insulin

74
Q

two major acute phase proteins

A

C-reactive protein (CRP)

serum amyloid P (SAP)

75
Q

C-reactive protein (CRP) and serum amyloid P (SAP) are acute phase proteins from the ______ family

A

pentraxin

76
Q

plasma concentrations of CRP and SAP are very low in healthy individuals but can increase up to ______ - fold during infections

A

1000

77
Q

what is responsible for increased levels of CRP and SAP?

A

tissue damage/infection –> phagocytes produce IL-1 and IL-6 –> liver increases synthesis of CRP and SAP

78
Q

CRP and SAP recognize ______ (found on bacteria) and _______ (found on apoptotic cells)

A

phosphorycholine

phosphatidylethanolamine

79
Q

CRP and SAP can activate complement by binding _____ and initiating the ______ pathway

A

C1q

classical

80
Q

C1q binds to CRP in the same way as C1q binds to ______ in classical complement pathway

A

IgM

81
Q

upon viral infection, viral nucleic acids and proteins are recognized by several

A

cellular TLRs

82
Q

TLR-mediated signaling activates transcription factors [the IRF (interferon regulatory factors) proteins] that stimulate the production of

A

Type I Interferons (IFN-alpha and IFN-beta)

83
Q

once virally infected cells secrete IFN-alpha and IFN-beta, they bind to receptors on infected cells inducing the expression of genes whose products enhance the cell’s susceptibility to

A

CTL-mediated killing

84
Q

IFN-alpha and IFN-beta produced by virus-infected cells can bind to membrane receptors on neighboring uninfected cells and activate ______ pathway that induces expression of genes whose products ______ with viral replication by the following ways:

  1. inhibition of viral protein synthesis
  2. degradation of viral RNA
  3. inhibition of viral gene expression and virion assembly
A

JAK-STAT signaling

interfere

85
Q

pathogen recognition through PRRs is an important bridge between

A

innate and adaptive immunity

86
Q

pathogen recognition through PRRs causes activation and maturation of

A

antigen-presenting cells (APCs)

87
Q

secreted cytokines (e.g. cytokine ______ ) assisted with development and maturation of T cell

A

IL-12

in absence of IL-12 –> humoral-mediated immunity???

88
Q

2 ways B cells are activated

A
  1. antigen recognition by B cell leads to activation
  2. molecules induced by innate immune responses to microbes (costimulator, complement fragment, etc.) leads to activation

Immunology (23 decks)

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