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Immuno Exam 3 > Immunity to Microbes > Flashcards

Immunity to Microbes Flashcards

1
Q

Defense against microbes is mediated by the effector mechanisms of _______ and _______ immunity.

A

Innate

Adaptive

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2
Q

The survival and ________ of microbes in a host are critically influenced by the ability of the microbes to evade or resist the effector mechanisms of immunity.

A

Pathogenicity

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3
Q

In many infections, tissue injury and disease may be caused by the host response to the microbe (_______ _______) rather than by the microbe itself.

A

Collateral damage

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4
Q

T/F. Inherited and acquired defects in innate and adaptive immunity are important causes of susceptibility to infections.

A

True

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5
Q

Many microbes establish _______, or persistent infections in which the immune response controls but does not eliminate the microbe and the microbe survives without propagating the infection.

A

Latent

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6
Q

The first step in primary infection with extracellular bacteria is a break in the ________ surface that allows the bacteria entry and proliferation.

A

Epithelial

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7
Q

The second step in primary infection with extracellular bacteria is when the surface lipopolysaccharide (LPS) may activate the ________ and ________ complement pathways or mannan-binding protein (MBP) the lectin pathway leading to bacterial lysis.

A

Alternative

Classical

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8
Q

In the second step of primary infection with extracellular bacteria, other complement activators operating at this stage include acute phase proteins _______ and _______. Acute phase proteins bind bacterial coat and activate complement.

A

CRP (C-reactive protein)

SAP (Serum amyloid protein)

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9
Q

Both CRP and SAP are known to bind bacterial surfaces (phosphocholine) and to bind the globular heads of C1q and activates the ________ pathway of complement.

A

Classical

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10
Q

In the third step of primary infection with extracellular bacteria, C3a and C5a bind to receptors on resident _______ cells and activate them.

A

Mast

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11
Q

Mast cell degranulation releases large amounts of _______ and _______ that enhances blood flow.

A

Histamine

Bradykinin

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12
Q

________, operating through H1 and H2 receptors, causes arteriolar vasodilation, venous constriction in some vascular beds, and increased capillary permeability. The actions of bradykinin are similar to this.

A

Histamine

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13
Q

The increased blood flow (due to mast cells: histamine and bradykinin) and local _______ are perceived as itchiness and irritation in the inflamed area.

A

Edema

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14
Q

In the fourth step of primary infection with extracellular bacteria, mast cells are the first to release cytokines and chemokines and together with bacterial-derived molecules (i.e., endotoxin) activate both the endothelium and the ________ via PRRs. Rolling and marginating ________ adhere to the vein wall.

A

Neutrophils

Neutrophils

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15
Q

In the fifth step of primary infection with extracellular bacteria, complement fragments (____ and ____) and chemokines (_____/_____) are potent neutrophil chemoattractants. Together with bacterial products such as fMLP, they attract neutrophils to the site (chemotaxis).

A

C5a
C3a
IL-8
CXCL8

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16
Q

In the sixth step of primary infection with extracellular bacteria, opsonized bacteria (C3b) are rapidly engulfed and killed by neutrophils and tissue macrophages. Immature _____ engulf and internalize bacteria (Ags) via PRRs (pattern recognition receptors – i.e., Toll-like receptors). Activated mature ______ migrate to the local LNs via the lymphatics.

A

DCs

DCs

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17
Q

In the seventh step of primary infection with extracellular bacteria, DCs enter local LNs and moves to the T cell zone. Local inflammation leads to up-regulation of adhesion molecules on _______ of lymph node, and lymphocytes enter directly from the blood.

A

HEV

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18
Q

Many lymphocytes become trapped, activated, and proliferate in the local inflamed LN. This leads to the consequent swelling and local _______ that manifested by the symptoms of swollen painful/tender LNs.

A

Hyperemia (increase of blood flow to tissue)

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19
Q

The homing of lymphocytes to peripheral LNs is initiated by an adhesive interaction between constitutively expressed ________ on lymphocytes and _______ constitutively displayed on HEV of LNs.

A

L-selectin

PNAd (Peripheral lymph node addressin)

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20
Q

In the eighth step of primary infection with extracellular bacteria, naive Th cells are recruited and activated by DCs in the lymph node. Naive T cells become differentiated towards effector _____, _____, or _____ cells according to the DC signals.

A

Th1
Th2
Th17

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21
Q

Activated Th cells migrate towards the _______ _______ and interact with Ag-activated B cells, promoting affinity maturation, and Ig class-switching of bacteria-specific Abs.

A

Germinal centers

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22
Q

Initially, ______ class Ab is produced, followed by clonal expansion and switching to other classes, i.e., _____ or _____ for mucosal pathogens by the engagement of CD40-CD40L.

A

IgM
IgG
IgA

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23
Q

In the ninth step of primary infection with extracellular bacteria, IgM is a very potent complement activator. After formation of multiple ______, bacteria are lysed by complement. Bacteria are also opsonized with _____ via IgM-activated complement (classical pathway) that increases phagocytosis.

A

MACs

C3b

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24
Q

Early antibacterial Ab production is of the IgM class. This relatively low affinity interaction is enhanced by the five adhesion sites on IgM, leading to higher ______ of the binding.

A

Avidity

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25
Q

In the tenth step of primary infection with extracellular bacteria, in the resolution of an infection, bacterial debris is removed by local ________ (M2 macrophages and neutrophils) or by antibody as soluble immune complexes.

A

Phagocytes

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26
Q

In the final step of primary infection with extracellular bacteria, upon elimination of pathogens, the immune responses are contracted and most of effector lymphocytes die via apoptosis. Protective mechanisms for future encounters are put in place by the laying down of _______ and _______ cells and long-lived _______ cells.

A

Memory B
Memory T
Plasma

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27
Q

T/F. Extracellular bacteria are capable of replicating outside host cells in the blood, connective tissues, epithelial surfaces, the GI tract etc.

A

True

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28
Q

Infections caused by pathogenic extracellular bacteria have two principal mechanisms:

1) Tissue damage is caused by ________ at the site of infection.
2) Bacteria produce ______ which have diverse pathologic effects.

A

Inflammation

Toxins

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29
Q

The bacterial toxins subdivided into:

    • _______ which are components of bacterial cell walls
    • _______ which are secreted by the bacteria
A

Endotoxins

Exotoxins

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30
Q

The ________ (LPS) of Gram-negative bacteria is a potent activator of macrophages, DCs, and endothelial cells.

A

Endotoxin

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31
Q

Many _______ are cytotoxic including diphtheria toxin (shuts down protein synthesis in infected cells), cholera toxin (interferes with ion/water transport), and tetanus toxin (inhibits neuromuscular transmission).

A

Exotoxins

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32
Q

Other exotoxins interfere with normal cellular functions without killing cells, and yet other exotoxins stimulate the production of ________ that cause disease.

A

Cytokines

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33
Q

The principal mechanisms of innate immunity to extracellular bacteria are…

A

Complement activation
Phagocytosis
Inflammation

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34
Q

Bacteria that express _______ on their surface may bind ______-binding lectin, which activates complement by the lectin pathway.

A

Mannose

Mannose

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35
Q

Bacterial ________ (Gram+ bacteria) and ______ (Gram- bacteria) activate the alternative and classical activation pathways.

A

Peptidoglycans

LPS

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36
Q

Blood acute phase proteins _____ and _____ can activate classical complement pathway.

A

CRP

SAP

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37
Q

Byproducts (C3a and C5a) stimulate _________ by recruiting and activating leukocytes.

A

Inflammation

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38
Q

Complement activation results in _________ and enhanced phagocytosis of the bacteria.

A

Opsonization

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39
Q

The ______ lyses bacteria (Neisseria) that are particularly susceptible to lysis.

A

MAC

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40
Q

The cleavage of C3b and C4b by _______ prevents them from forming active convertases and requires cofactor activity. These cofactors include the membrane-bound ______, ______, ______, and ______.

A 
Factor I 
MCP
CR1
FH
C4BP
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41
Q

Proteins ______, CR1, and C4BP inhibit assembly of new C3 convertases and shorten the half-life of the preformed convertases, limiting their ability to participate in complement activation:

Classical pathway – ______, ______, and ______
Alternative pathway – ______, ______, and ______

A

DAF
DAF; CR1; C4BP
DAF; Factor H; CR1

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42
Q

The ______ is the lytic complex of complement and its assembly can be inhibited by the membrane-bound ______-inhibitory protein, or CD59.

A

MAC

MAC

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43
Q

The major mechanism used by bacteria to evade humoral immunity is variation of surface ______.

A

Ags

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44
Q

Innate immune evasion by extracellular bacteria includes:

    • Inhibition of ________ activation
    • Resistance to phagocytosis
    • Scavenging of reactive _______ species
A

Complement

Oxygen

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45
Q

________ immunity is a major protective response against extracellular bacteria. It functions to block infection, to eliminate the microbes, and to neutralize their toxins.

A

Humoral

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46
Q

The effector mechanisms of Abs include:

    • Toxin _________
    • ________ and phagocytosis
    • Complement activation by the classical pathway
A

Neutralization

Opsonization

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47
Q

Abs responses against extracellular bacteria are directed against cell wall _____ and secreted and cell-associated toxins.

A

Ags

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48
Q

_________ bacteria rich TI polysaccharide Ags are primarily eliminated by Ab-mediated immunity.

A

Encapsulated

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49
Q

The protein Ag of extracellular bacteria also activate…

A

CD4+ helper T cells

50
Q

_____ cells induced by these microbes promote local inflammation and recruit neutrophils and monocytes at sites of bacterial infection. Genetic defects in _____ development have increased susceptibility to bacterial and fungal infections, with formation of multiple skin abscesses.

A

Th17

Th17

51
Q

Bacterial also induce _____ cells and _____ produced by the cells activates macrophages to destroy phagocytize microbes.

A

Th1

IFN-y

52
Q

______ may also stimulate production of opsonizing and complement-fixing IgG Abs.

A

IFN-y

53
Q

The principal injurious consequences of host responses to extracellular bacteria are ________ and _______ _______.

A

Inflammation

Septic shock

54
Q

T/F. Inflammatory reactions are usually self-limited and controlled.

A

True

55
Q

______ ______ is a severe pathologic consequence of disseminated bacterial infection (sepsis) by some Gram-negative and Gram-Positive bacteria.

A

Septic shock

56
Q

This is characterized by circulatory collapse and disseminated intravascular coagulation.

A

Septic shock syndrome

57
Q

The early phase of sepsis and septic shock is caused by ________ produced by macrophages that are activated by bacterial cell wall components.

A

Cytokines

58
Q

Cytokines secreted cause the systemic manifestations of the infection and stimulate the production of _________ proteins.

A

Acute-phase (CRP; SAP)

59
Q

The same reactions of neutrophils and macrophages that function to eradicate the infection also cause tissue damage by local production of reactive _______ species and ________ enzymes.

A

Oxygen

Lysosomal

60
Q

________ release a diverse range of products implicated in the pathogenesis of sepsis.

A

Macrophages

61
Q

Many macrophage products are involved in the regulation of each other:

– ______ up regulates TF (tissue factor) and iNOS (nitric oxide synthase)

– ______ induces IFN-y, which in turn further activates macrophages

A

TNF-a

IL-18

62
Q

______ is a global suppressor of macrophage function.

A

IL-10

63
Q

MIP and MCP are chemokines that mobilize and activate inflammatory cells, especially ________. They also activate ________.

A

Neutrophils

Macrophages

64
Q

Certain bacterial toxins called _________ bind to the class II MHC outside the peptide-binding groove. Simultaneously, these bind to the variable region of different TCR beta chains, regardless of the peptide specificity of the TCR.

A

Superantigens (SAgs)

65
Q

Because many T cells express a TCR beta chain from a particular VB family, SAgs can activate a large number of T cells causing _________ T cell activation.

A

Polyclonal

66
Q

The staphylococcal SAgs are potent GI toxins responsible for staphylococcal _______ _______.

A

Food poisoning

67
Q

This is caused by S. aureus and can be considered a capillary leak syndrome.

A

Toxic shock syndrome (TSS)

68
Q

Streptococcal TSS is caused by ________ and it is the most severe form of invasive streptococcal infection.

A

S. pyogenes

69
Q

This disease is an acute multi-system vasculitis of unknown etiology – evidence suggest that it is a SAg-mediated disease.

A

Kawasaki disease (KD)

70
Q

It has been proposed that SAgs might contribute to the pathogenesis of _________ disease by activating T cells that are specific for self Ags.

A

Autoimmune

71
Q

This is a post-infection cause of preventable pediatric heart disease. It is caused by Abs against Ags from Streptococcus pyogenes that cross-react (molecular mimicry) with myosin and laminin on heart valves.

A

Acute rheumatic fever (ARF)

72
Q

Intracellular bacteria and viruses are able to survive and replicate within host cells where they are inaccessible to circulating Abs. An elimination of these bacteria requires the mechanisms of __________ immunity.

A

Cell-mediated

73
Q

T/F. In intracellular bacterial and viral infections the host responses do not cause tissue injury.

A

False. In many intracellular bacterial and viral infections the host responses also cause tissue injury.

74
Q

In a primary viral infection, the virus infects ________ cells and replicates among them.

A

Epithelial

75
Q

The effect of intracellular viral infection is the activation of cytokine and cytokine-receptor genes, especially the ________ _______ (i.e., IFN-a).

A

Type I interferons

76
Q

Local effects of IFN-a are inhibition of viral gene replication, and up-regulaton of _______ molecules.

A

MHC class I

77
Q

Viral _______ are expressed in the MHC class I peptide-binding groove.

A

Peptides

78
Q

______ cells may be recruited at two points during the virus infection. They exhibit an innate (early in the course of infection) antiviral role following activation by epithelium-derived IFN-a.

A

NK

79
Q

At a later stage of infections, NK cells are activated by cytokines IFN-y and IL-2 produced by _____ cells specific for the virus.

A

Th1

80
Q

Viral infection results in cell death and viral replication. Components of viruses (i.e., single-stranded RNA) activate ______ and locally released cytokines and chemokines amplify the activation of macrophages and professional APCs. These cells engulf cellular debris and present viral proteins.

A

DCs

81
Q

Professional APCs (i.e., tissue DCs such as _________ cells in the skin) transport Ag to local LNs via lymphatics.

A

Langerhans

82
Q

Cytokines up-regulate endothelial cell expression of adhesion molecules such as ______. Chemokines (i.e., IL-8/CXCL8) begin to attract cells through the endothelium towards the site of infection.

A

ICAM-1

83
Q

IL-1 and TNF-a locally produced by macrophages and T cells enter bloodstream and have systemic effects of ______ and arthralgia/myalgia.

A

Fever

84
Q

Naive T cells possessing TCRs complementary to the class II MHC molecule/viral peptide complex are activated and become ______ cells.

A

Th1

85
Q

Naive B cells acquire viral Ags through attachment to surface ______ or ______.

A

IgM

IgD

86
Q

Antiviral _____ are produced as a result of primary Ab response.

A

IgM

87
Q

Ag-activated B cells process and present viral peptides to Th cells (either Th2 or Th1) from which they receive positive growth and differentiation signals. B cells differentiate and class switch, leading later to production of high _______ antiviral IgG (secondary Ab response).

A

Affinity

88
Q

A viral peptide is presented by class II MHC molecules to a complementary ______ on a Th cell. The interaction is stabilized by CD4/class II MHC and CD80;86/_____, which also provides co-stimulatory signals to the Th cell.

A

TCR

CD28

89
Q

Th1 cells recruit and stimulate virus-specific ______ by providing IL-2 for proliferation of CD8+ T cells.

A

CTLs (cytotoxic T lymphocytes)

90
Q

The CTLs recognize virus peptides cross-presented by ______. The same viral epitopes will be presented within class I MHC on the surface of infected target cells.

A

DCs

91
Q

Effector Th cells and CTLs leave the LN via the draining lymphatics and ultimately enter the blood. At this stage their key attributes are:

1) Virus-specific ______
2) Up-regulated adhesion molecules (LFA-1), to allow migration into the inflamed tissues
3) Up-regulated production of cytokines

A

TCRs

92
Q

Virus-specific CTLs migrate from the blood into peripheral tissue. CTLs recognize viral Ags presented within _______ _______ on virally infected cells and kill them.

A

Class I MHC

93
Q

In the tissue, Th1 cells, CTLs and B cells organize the local antiviral immune response:

– Th1-derived _____ activates phagocytosis by macrophages

– Abs facilitate phagocytosis via ______ and ______

A

IFN-y
FcR
CR1

94
Q

Virus-infected cells secrete viral proteins after their death. These proteins may be neutralized or removed by ______ in the form of immune complexes.

A

Ab

95
Q

Ab may guide Fc receptor-expressing ______ cells that culminates in _______.

A

NK

ADCC (Antibody-Dependent Cell-Mediated Cytotoxicity)

96
Q

After resolution of the infection, virus-specific memory T and B cells reside long term in lymph nodes, spleen, and bone marrow. ________ cells ensure long-term circulation of protective virus-neutralizing Abs.

A

Plasma

97
Q

________ immunity – is mediated by phagocytes and NK cells interactions among which are mediated by IL-12 (DCs and macrophages) and IFN-y (NK cells). May control bacterial growth, but elimination of the bacteria requires _______ immunity.

A

Innate

Adaptive

98
Q

Adaptive immunity is ________ immunity (CTLs) in which Th1 cell-produced IFN-y activates phagocytes to eliminate the microbes.

A

Cell-mediated

99
Q

Products of these bacteria are recognized by TLRs and cytoplasmic proteins of the NOD-like receptors resulting in activation of DCs, macrophages, and neutrophils. ________ ingest and destroy intracellular microbes.

A

Phagocytes

100
Q

The resistance of pathogenic bacteria to degradation within phagocytes is overrun by NK cell-produced ______.

A

IFN-y

101
Q

Activated DCs and macrophages produce ______ and ______ which active NK cells. The NK cells produce _____, which in turn promotes killing of the phagocytize bacteria by macrophages.

A

IL-12
IL-15
IFN-y

102
Q

_________ may survive in phagosomes by preventing acid-containing lysosomes from fusing with phagosomes and creating mature phagolysosomes.

A

M. tuberculosis

103
Q

CD4+ Th1 cells respond to class II MHC-associated M. tuberculosis Ags and produce ______, which activates macrophages to destroy the microbes in phagosomes.

A

IFN-y

104
Q

CD8+ T cells respond to class I MHC-associated peptides derived from ________ Ags (cross-presenting) and kill the infected cells.

A

Cytosolic

105
Q

In _________ pathway, proteins from intracellular pathogens, such as viruses, are degraded by the proteasome and the resulting peptides are shuttled into the ER by TAP proteins.

A

Endogenous

106
Q

In endogenous pathway, these peptides are loaded onto MHC class I molecules and the complex is delivered to the cell surface, where it stimulates _______ that kill the infected cells.

A

CTLs

107
Q

In _________ pathway, extracellular pathogens are engulfed by phagosomes. Inside the phagosome, the pathogen-derived peptides are loaded onto MHC class II molecules, which activate Th cells that stimulate the production of Abs.

A

Exogenous

108
Q

Some peptides form the exogenous pathway can also be presented on MHC class I molecules, this is called _______-_______.

A

Cross-presentation

109
Q

Immune evasion by intracellular bacteria can be by:

    • Inhibition of phagolysosome formation
    • Inactivation of reactive oxygen and nitrogen species
    • Disruption of phagosome membrane, escape into ______
A

Cytoplasm

110
Q

Naive CD4+ T cells may differentiate into _____ cells, which activate phagocytes to kill ingested microbes or _____ cells, which inhibit this classical pathway of macrophage activation.

A

Th1

Th2

111
Q

T/F. The Th1/Th2 balance may influence the outcome of infections.

A

True

112
Q

Fungi are recognized by PRRs (TLRs and C lectin-like receptors) binding the ______. The detection of Beta-glucan by ______ is also important.

A

PAMPs

Dectin 1

113
Q

After fungi recognition, then occurs differentiation of Th1, Th2, and Th17 cells and production of cytokines. Cytokines ______ and _____ + _____ have important differentiation and activation roles for activation of Th1 and Th17 responses.

A

IL-12

TGF-B; IL-6

114
Q

In general, Th1 responses are required for clearance of a fungal infection, while Th2 responses usually results in ________ to infection.

A

Susceptibility

115
Q

For fungal infections, Th1 (IFN-y) and Th17 (IL-17, IL-22) cytokines further amplify an inflammation and innate immunity. Specific ______ cells (Abs) are less important.

A

Th2

116
Q

The macrophage mannose receptor (MR) has historically been considered the major receptor involved in the nonopsonic recognition of fungi. _______ is a recently discovered PRR that plays an important role in anti fungal innate immunity.

A

Dectin-1

117
Q

Recent data suggest that Dectin-1 and _____/_____ signaling combine to enhance the responses triggered by fungi.

A

TLR2/TLR6

118
Q

Dectin-1 is a specific receptor for ________ expressed on macrophages.

A

Beta-glucans

119
Q

Beta-glucans are polysaccharide _______ that contain only glucose as structural components.

A

PAMPs

120
Q

Dectin-1 binds and internalizes Beta-glucans and mediates activation of ______ and subsequent secretion of pro inflammatory cytokines and production of reactive oxygen species (ROS).

A

NF-kB

Immuno Exam 3 (6 decks)

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