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Immunity > Innate Immunity II > Flashcards

Innate Immunity II Flashcards

1
Q

As with many or most immune cells, NK cells can be stimulated for growth and activation by

A

Cytokines

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2
Q

Which type of cytokine stimulates growth and activation of NK cells?

A

IL-12, Type I interferon

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3
Q

What are the two important substances contained in the granules of NK cells?

A

Perforin and granzymes

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4
Q

Facilitates the entry into target cells of other substances from the NK cell

A

Perforin

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5
Q

Enzymes that enter the cytoplasm of target cells and initiate signaling cascades leading to cell death by apoptosis

A

Granzymes

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6
Q

Thus, NK cells have several primary roles: in the early phases of a viral infection, before there are virus-specific CTLs, NK cells can

A

Kill virus-infected cells

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7
Q

NK cells can also kill cells with

A

Intracellular microbes

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8
Q

Released by activated NK cells activates macrophages for more efficient phagocytosis and killing of bacteria or intracellular targets such as cells carrying intracellular pathogens, such as Listeria monocytogenes

A

IFN-γ

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9
Q

Form a surveillance and antigen-capture network in epithelia and subepithelial tissues and in a number of other organs

A

Dendritic Cells

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10
Q

The majority of DCs are called “conventional” DCs, and these include the

A

Langerhans cells in the skin

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11
Q

Their primary function is to recognize and/or capture antigen, either microbes or free antigens

A

Conventional DCs

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12
Q

Have a strong array of TLRs and other pattern-recognition receptors

A

Conventional DCs

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13
Q

After recognizing and capturing antigens, DCs have which 2 major effects?

A
  1. ) Produce pro-inflammatory cytokines

2. ) Travel to lymph nodes to present antigen to T cells

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14
Q

Set off antigen-specific T cell responses and serving as a key link to the adaptive immune response

A

Conventional DCs

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15
Q

A second, more rare, but critical type of dendritic cell is the

A

Plasmactytoid dendritic cell (pDC)

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16
Q

These cells specifically have high levels of TLR 3, 7 and 9 in the endosome, whereby they can respond with great sensitivity to single- and double-stranded RNA, and also to DNA, which are characteristic of viruses

A

Plasmactytoid dendritic cell (pDC)

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17
Q

pDCs have high levels of TLRs

A

3, 7, and 9

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18
Q

In response, the pDCs turn on very strong production of the anti-viral family of

A

Type I interfurons (especially IFN-α, and IFN-β)

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19
Q

These IFNs (in contrast to gamma interferon; IFN-γ) have 2 main effects: (1) they have a direct

A

Anti-viral effects

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20
Q

Also, these Type I interferons modulate a host of cellular reactions by cells of the immune system, making the Type I IFNs an important link between

A

Innate and adaptive immunity

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21
Q

Primarily associated with immunity to multi-cellular parasites and to allergy and asthma, but they are also important for innate immunity

A

Mast Cells

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22
Q

They are present in the skin and mucosal epithelium, where they are often found adjacent to the microvasculature and nerves

A

Mast Cells

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23
Q

The mast cells have numerous cytoplasmic granules containing inflammatory mediators including

A

Histamine

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24
Q

Mast cells also produce lipid mediators, such as

A

Prostaglandins and cytokines

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25
Q

Mast cells contain a number of pathogen recognition receptors, including most

A

TLRs

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26
Q

Mast cells contain a number of pathogen recognition receptors, including most TLRs, which can be stimulated by their ligands in vitro to induce

A

Degranulation and cytokine release

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27
Q

The location of mast cells, and the presence of important PRRs suggests an important role in

A

Innate immunity

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28
Q

Recognition molecules critical to innate immunity are also found in the serum and in tissues, and help

A

Tag or destroy molecules

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29
Q

Recognition molecules bind to microbes, acting as

A

Opsonins

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30
Q

This enhances their recognition by cellular receptors on macrophages, neutrophils and dendritic cells because these cells have receptors for these

A

Opsonins

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31
Q

May initiate or promote inflammatory responses that attract phagocytes, and/or they may participate directly in killing of pathogens

A

Soluble recognition molecules

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32
Q

Perhaps the best known and most important soluble recognition and effector molecules are those of the

A

Complement system

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33
Q

This system is composed of roughly 20 proteins in normal human serum, most of which are produced in the liver

A

Complement proteins

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34
Q

Functions in defense against pathogens, and functions in homeostasis, particularly recognizing damaged or apoptotic cells or their components and helping dispose of them without triggering inflammation

A

Complement system

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35
Q

Functions to opsonize (coat) and tag microbes for phagocytosis and killing

A

Complement system

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36
Q

The complement system mobilizes and recruits phagocytes to the site of

A

Infection

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37
Q

In some cases, the complement system functions to directly kill

A

Pathogens

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38
Q

What are the three pathways to trigger the cascade of reactions of the complement system?

-Once triggered, converge to a common pathway

A

Classical, alternative, and lectin pathways

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39
Q

The “classical pathway”, so-called because it was the first pathway recognized and described, is initiated by

A

Antibody binding to pathogen

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40
Q

Because it involves antigen-specific antibodies, it is often considered part of adaptive immunity

A

Classical pathway

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41
Q

The alternative and lectin pathways do not depend on pathogen-specific

A

Antibodies

42
Q

The 3 pathways differ primarily in their early events, but then connect through the critical protein

A

C3

43
Q

Is always going on, because it begins with the spontaneous hydrolysis of complement protein C3, which is present in high concentrations in serum (and in tissue)

A

Alternative tissue

44
Q

The C3 products are

A

C3a and C3b

45
Q

Highly reactive (and very short-lived), and can react with and covalently bind to bacterial or fungal polysaccharides or proteins

A

C3b

46
Q

If no targets of active C3b are nearby, the reactive group on C3b quickly hydrolyzes and the C3b becomes

A

Inactive

47
Q

However, C3b bound to cells binds another serum protein called

A

Factor B

48
Q

Cleaved by a plasma protease to form a “Bb” fragment, so there is now a C3bBb complex on the bacterial surface

A

Factor B

49
Q

This creates a powerful amplification of both the amount of protease activity to activate C3, and also to “decorate” or tag the bacteria or other targets with a lot of complement, particularly

A

C3b

50
Q

With multiple C3b molecules attached, the cells become targets for

A

Phagocytes

51
Q

Opsinizes pathogens

A

C3b

52
Q

Some membrane-bound C3bBb complexes can bind a 2nd molecule of C3b, changing its proteolytic specificity so it becomes a

A

C5 convertase

53
Q

Can cleave C5, producing the fragments C5b and C5a

A

C5 convertase

54
Q

The larger C5b piece can stick to the cell surface and recruit components (C6, 7, 8 and 9; this is known as the

A

Membrane attack complex (MAC)

55
Q

This forms a pore in some cells, and may be capable of lysing some cells, particularly bacteria of the

A

Neisseria genus (species of which can cause meningitis or gonorrhea)

56
Q

The cleavage of both C3 and then C5 (and C4 in the other pathways) releases the smaller, soluble protein fragments

A

C5a and C3b

57
Q

In response, many inflammatory cells chemotax toward the site of infection, and may be activated for

A

Inflammation

58
Q

The fragments can also cause degranulation of mast cells, releasing “inflammatory mediators”, including

A

Histamine and leukotrines

59
Q

Have critical effects in acute inflammation

A

Leukotrines

60
Q

If complement is extensively activated in the bloodstream, large amounts of C3a/C5a are produced, and a large number of mast cells will be stimulated

A

Degranulate

61
Q

These may release sufficient inflammatory mediators to produce systemic vasodilation, loss of blood pressure, and shock, i.e., anaphylaxis, so that these fragments are called

A

Anaphylatoxins

62
Q

Takes advantage of the fact that carbohydrates on the surface of healthy human cells may differ from those on pathogens

A

Lectin pathway

63
Q

The best known example of the initiation of the Lectin pathway is when

A

Mannan-Binding Lectin (MBL) recognizes terminal glycolipids and glycoproteins on bacteria or fungi

64
Q

After MBL binds to the bacterial (or fungal) sugar on the bacterium, it recruits specific proteases (“MBL-associated serine proteases”; MASPs) that then cleave proteins

A

C4 and C2

65
Q

This produces cell-bound

A

C4b2a, a second C3 “convertase”

66
Q

Cleaves C3 to C3b and C3a

A

C4b2a

67
Q

Some of the C3b can join bind to the C4b2a to form a C5 convertase, analogous to that of the alternative pathway, leading to the same outcomes as from the

A

Alternative pathway

68
Q

As mentioned above, the “classical pathway” relies on an antigen-specific antibody that recognizes and binds to an antigen of the pathogen. The bound antibody is then recognized by

A

Complement C1

69
Q

Subunits of complement C1 cleave C4 and C2, creating

A

C3 convertase

70
Q

Some of cleaved C3b binds to C4bC2a to form the

A

C5 convertase

71
Q

An example of extending the older complement system of innate immunity and coupling it to antibodies, produced by the B cells of adaptive responses

A

Classical pathway

72
Q

Because of the requirement for pathogen-specific antibodies, this pathway is generally engaged only on repeated or prolonged encounter with a pathogen, when specific antibodies have been produced

A

Classical Pathway

73
Q

Can produce increased susceptibility to bacterial infections, particularly early in life

A

C3 deficiency

74
Q

Variable from asymptomatic to increased susceptibility to bacterial infection. Can be associated with systemic lupus erythematosus

A

C2 and C4 deficiency

75
Q

Increased susceptibility to Neisseria

A

C9 deficiency

76
Q

Increased complement activation → Reduced levels of C3 (“depletion”) → increased infection.

A

Factor I or Factor H deficiency

77
Q

Complement also serves an important role in helping to clear complexes of

A

Antigen and antibody

78
Q

Have complement receptors and bind circulating immune complexes

A

Erythrocytes

79
Q

The complexes bound to red cells are phagocytosed and destroyed by macrophages in the

A

Liver and spleen

80
Q

Alternatively, if the complexes reach lymph nodes and are trapped by dendritic cells, this is a potent stimulus to an

A

Immune response

81
Q

Persons genetically defective in early components of complement (C1 through C3) have an elevated frequency of

A

Autoimmune disease

82
Q

Antibody-antigen complexes (“immune complexes”) lodged in tissue create damage by

A

Complement activation

83
Q

A major target of such damage, since it filters these complexes from blood

A

The kidney

84
Q

In autoimmune disease, because a component of the body is the antigen, immune complexes are

A

Continuously formed

85
Q

Ongoing or very high level deposition of an antigen-antibody complex, can lead to high levels of complement recognition and activation, leading to cellular damage, thereby contributing to life-threatening

A

Kidney Damage

86
Q

There are other soluble recognition and effector molecules. One important family is the

A

Pentraxins

87
Q

Include some of the proteins that are produced during inflammation, called acute-phase proteins, or acute-phase reactants

A

Pentraxins

88
Q

What are two examples of pentraxins?

A

C-reactive protein (CRP) and serum amyloid protein (SAP)

89
Q

These can activate complement C1, feeding into the complement pathway

A

CRP and SAP

90
Q

In addition, these proteins, particular CRP sometimes serve diagnostically as important “biomarkers” for

A

Inflammation

91
Q

Proteins that act as signals with the immune system (and some also during development and other processes)

A

Cytokines

92
Q

In the pro-inflammatory pathways, the major cytokines are

A

TNF-α, IL-1, and IL-6

93
Q

During viral infections, the main signal released are

A

Type I and Type III interferons

94
Q

The major outcomes of activating the components of innate immunity are either an

A

Inflammatory response or an immune response

95
Q

Includes the recruitment of leukocytes, and the phagocytosis and killing of microbes by activated phagocytes, as well as stimulating elements of adaptive immunity to both produce a stronger response and initiate immunological memory

A

Inflammatory Response

96
Q

Depends on the production of Type I and Type III interferons (primarily IFN-αs and IFN-β) by cells infected by virus

A

Antiviral response

97
Q

Is NOT a Type I IFN, does not have a major role in the antiviral response, is produced under different conditions and has distinct biological activities

A

Gamma interferon, IFN-γ

98
Q

Can activate almost all nucleated cells

A

Type I IFNs

99
Q

Primarily promote antiviral responses on epithelial cells of mucosal tissue, which are a common sites of virus invasion

A

Type III IFNs

100
Q

All nucleated mammalian cells can respond to viruses through their various

A

PRRs

Immunity (33 decks)

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