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Summer Immuno Lecture 2

front 1

Which organ normally produces most complement proteins?
A. Spleen
B. Liver
C. Thymus
D. Bone marrow

back 1

B. Liver

front 2

A researcher measures complement proteins in serum. Which protein should be most abundant?
A. C1
B. C5
C. C9
D. C3

back 2

D. C3

front 3

In the alternative complement pathway, C3 is continuously split into which products?
A. C3a and C3b
B. C4a and C4b
C. C5a and C5b
D. C2a and C2b

back 3

A. C3a and C3b

front 4

Which C3 fragment is highly reactive after spontaneous C3 breakdown?
A. C3a
B. C4b
C. C3b
D. C5a

back 4

C. C3b

front 5

C3b rapidly binds chemical groups on nearby bacterial surfaces. Which groups are targeted?
A. Amino or hydroxyl
B. Sulfhydryl or methyl
C. Phosphate or carboxyl
D. Aldehyde or ketone

back 5

A. Amino or hydroxyl

front 6

If C3b fails to bind a target group quickly, it is neutralized. What is the approximate time window?
A. 6 seconds
B. 60 seconds
C. 6 microseconds
D. 60 microseconds

back 6

D. 60 microseconds

front 7

Free C3b that misses a bacterial surface is neutralized by which molecule?
A. Oxygen
B. Water
C. Glucose
D. Albumin

back 7

B. Water

front 8

After C3b stabilizes on a bacterial surface, which complement protein binds next?
A. C5
B. C9
C. B
D. MASP

back 8

C. B

front 9

After factor B binds stabilized C3b, which protein clips factor B?
A. D
B. C9
C. C5
D. MBL

back 9

A. D

front 10

Cleavage of factor B on surface-bound C3b forms which complex?
A. C3bC5b
B. C5b678
C. C4b2a
D. C3bBb

back 10

D. C3bBb

front 11

C3bBb enzymatically cleaves additional C3 molecules. What type of enzyme is C3bBb?
A. Ligase
B. Convertase
C. Polymerase
D. Kinase

back 11

B. Convertase

front 12

In the alternative pathway, C3bBb primarily cleaves which complement protein?
A. C1
B. C2
C. C3
D. C9

back 12

C. C3

front 13

C3bBb generates more C3b, which can form more C3bBb. What does this create?
A. Positive feedback
B. Negative feedback
C. Competitive inhibition
D. Clonal deletion

back 13

A. Positive feedback

front 14

C3bBb can bind another molecule to become a C5-cleaving complex. Which molecule is added?
A. C1q
B. C4b
C. MASP
D. C3b

back 14

D. C3b

front 15

The C3bBb-C3b complex cleaves which complement protein?
A. C3
B. C5
C. C7
D. C9

back 15

B. C5

front 16

C5 cleavage produces which two fragments?
A. C5a and C5b
B. C3a and C3b
C. C4a and C4b
D. C6a and C6b

back 16

A. C5a and C5b

front 17

Which complement fragment initiates membrane attack complex assembly?
A. C3a
B. C4b
C. C5b
D. C5a

back 17

C. C5b

front 18

C5b combines with which proteins to form the MAC?
A. C1, C2, C4, C9
B. C3, C4, C5, C6
C. C2, C3, C4, C5
D. C6, C7, C8, C9

back 18

D. C6, C7, C8, C9

front 19

In MAC formation, which components form the membrane-anchoring stalk?
A. C3bBb only
B. C5b, C6, C7, C8
C. C3a, C5a, C9
D. MBL, MASP, C3b

back 19

B. C5b, C6, C7, C8

front 20

Which MAC component forms the membrane pore?
A. C9
B. C8
C. C5a
D. C3b

back 20

A. C9

front 21

A gram-negative bacterium dies after complement forms a pore through its membrane. Which outcome occurred?
A. Antigen presentation
B. Thymic selection
C. Bacterial lysis
D. Class switching

back 21

C. Bacterial lysis

front 22

Spontaneous C3 breakdown is central to which pathway?
A. Classical pathway
B. Lectin pathway
C. Coagulation pathway
D. Alternative pathway

back 22

D. Alternative pathway

front 23

In the alternative pathway, what happens immediately after C3b stabilizes on bacteria?
A. B binds C3b
B. C9 forms pores
C. MBL binds mannose
D. C5b recruits C6

back 23

A. B binds C3b

front 24

In the alternative pathway, what does factor D do?
A. Cleaves C5 directly
B. Cleaves bound B
C. Blocks C9 attachment
D. Binds bacterial mannose

back 24

B. Cleaves bound B

front 25

What is the main enzymatic function of C3bBb?
A. Cleaves factor D
B. Degrades C9 pores
C. Cleaves C3
D. Activates antibodies

back 25

C. Cleaves C3

front 26

What is the main enzymatic function of C3bBb-C3b?
A. Cleaves C3 only
B. Degrades C3bBb
C. Inactivates C3b
D. Cleaves C5

back 26

D. Cleaves C5

front 27

Which sequence best describes terminal MAC assembly?
A. C5b recruits C6-C9
B. C3a recruits C5a-C9
C. C3b recruits B-D-C9
D. MBL recruits MASP-C9

back 27

A. C5b recruits C6-C9

front 28

Human cells avoid complement injury partly because blood enzymes inactivate which molecule?
A. C5a
B. C9
C. C3b
D. MASP

back 28

C. C3b

front 29

Which cell-surface protein accelerates C3b inactivation?
A. CD59
B. MCP
C. MBL
D. C9

back 29

B. MCP

front 30

What is the role of membrane cofactor protein?
A. Opens bacterial pores
B. Clips factor B
C. Binds bacterial mannose
D. Accelerates C3b inactivation

back 30

D. Accelerates C3b inactivation

front 31

Which cell-surface protein accelerates C3bBb destruction?
A. DAF
B. MCP
C. MBL
D. C5b

back 31

A. DAF

front 32

Decay accelerating factor protects host cells by promoting which event?
A. C5b stabilization
B. C9 polymerization
C. C3bBb destruction
D. C3a chemotaxis

back 32

C. C3bBb destruction

front 33

CD59 is also known by which name?
A. Properdin
B. Protectin
C. Factor D
D. Factor B

back 33

B. Protectin

front 34

CD59 protects host cells by preventing which event?
A. C3 cleavage
B. C5a release
C. Factor B binding
D. C9 attachment

back 34

D. C9 attachment

front 35

The central recognition molecule in the lectin pathway is which protein?
A. MBL
B. MASP
C. C3bBb
D. CD59

back 35

A. MBL

front 36

Mannose-binding lectin is central to which activation pathway?
A. Classical
B. Alternative
C. Lectin
D. Terminal

back 36

C. Lectin

front 37

In blood, mannose-binding lectin binds which associated protein?
A. Factor B
B. MASP
C. C9
D. C5b

back 37

B. MASP

front 38

In the lectin pathway, MBL attaches to which bacterial surface sugar?
A. Glucose
B. Galactose
C. Fructose
D. Mannose

back 38

D. Mannose

front 39

In the lectin pathway, which component acts as the convertase?
A. MASP
B. MBL
C. C9
D. MCP

back 39

A. MASP

front 40

In the lectin pathway, MASP clips which complement protein?
A. C5
B. C9
C. C3
D. Factor B

back 40

C. C3

front 41

The classical pathway depends on which immune molecule?
A. Mannose
B. C3bBb
C. B2-microglobulin
D. Antibody

back 41

D. Antibody

front 42

Which pathway is antibody-independent?
A. Classical pathway
B. Alternative pathway
C. Fc receptor pathway
D. Plasma cell pathway

back 42

B. Alternative pathway

front 43

C3b can be clipped into an inactive opsonin. What is it called?
A. iC3b
B. C3a
C. C5b
D. C9

back 43

A. iC3b

front 44

Which statement best describes iC3b?
A. Active C5 convertase
B. MAC pore protein
C. Inactive opsonin
D. Potent anaphylatoxin

back 44

C. Inactive opsonin

front 45

iC3b still helps immune defense mainly by promoting which process?
A. Chemotaxis
B. Opsonization
C. Neutralization
D. Class switching

back 45

B. Opsonization

front 46

Which complement fragments help form MACs?
A. C3a and C5a
B. C4a and C5a
C. MASP and MBL
D. C3b and C5b

back 46

D. C3b and C5b

front 47

Which complement fragments act as chemoattractants?
A. C3a and C5a
B. C3b and C5b
C. C6 and C7
D. C8 and C9

back 47

A. C3a and C5a

front 48

C3a and C5a recruit immune cells toward inflammation. What is this function called?
A. Opsonization
B. Neutralization
C. Chemotaxis
D. Phagocytosis

back 48

C. Chemotaxis

front 49

Which complement fragment is especially powerful as a chemoattractant?
A. C3b
B. C5a
C. C5b
D. C9

back 49

B. C5a

front 50

C5a is especially powerful at attracting which immune cells?
A. Plasma cells
B. Erythrocytes
C. Megakaryocytes
D. Macrophages

back 50

D. Macrophages

front 51

C3a and C5a are also classified as what?
A. Anaphylatoxins
B. Immunoglobulins
C. Opsonins
D. Convertases

back 51

A. Anaphylatoxins

front 52

C3a and C5a can contribute to which systemic reaction?
A. Hemolytic anemia
B. Neutropenic fever
C. Anaphylactic shock
D. Thymic aplasia

back 52

C. Anaphylactic shock

front 53

Which cells are considered professional phagocytes?
A. B cells and T cells
B. Eosinophils and basophils
C. Plasma cells and mast cells
D. Macrophages and neutrophils

back 53

D. Macrophages and neutrophils

front 54

Which professional phagocyte acts as a sentinel cell in tissues?
A. Neutrophil
B. Macrophage
C. B cell
D. Platelet

back 54

B. Macrophage

front 55

Where are macrophage sentinel cells typically positioned?
A. Below exposed tissue surfaces
B. Inside erythrocyte cytoplasm
C. Within antibody constant regions
D. Attached to C9 pores

back 55

A. Below exposed tissue surfaces

front 56

Macrophage sentinels are especially found near tissues exposed to what?
A. Bone marrow
B. Thymic cortex
C. External environment
D. Red pulp

back 56

C. External environment

front 57

A C3 molecule spontaneously breaks apart near a bacterial membrane. Why must this occur very close to the target?
A. C3a binds only nuclei
B. C3b is rapidly neutralized
C. C9 blocks bacterial binding
D. MASP destroys C3b

back 57

B. C3b is rapidly neutralized

front 58

A tissue macrophage is primed by inflammatory cytokines and begins presenting antigen to helper T cells. Which molecule is upregulated?
A. Class I MHCs
B. IgE receptors
C. Class II MHCs
D. C9 channels

back 58

C. Class II MHCs

front 59

A resting macrophage becomes an antigen-presenting cell after activation. What change best explains this?
A. Increased class II MHC
B. Decreased lysosome number
C. Loss of cytokine secretion
D. Reduced antigen display

back 59

A. Increased class II MHC

front 60

A macrophage is exposed to IFN-gamma during infection. What is the expected functional result?
A. Antibody secretion
B. Neutrophil apoptosis
C. Hemoglobin production
D. Macrophage priming

back 60

D. Macrophage priming

front 61

Which cytokine is best known for priming resting macrophages?
A. IL-4
B. IFN-gamma
C. IL-10
D. Histamine

back 61

B. IFN-gamma

front 62

IFN-gamma is produced mainly by which cells?
A. Plasma cells and eosinophils
B. Mast cells and basophils
C. Neutrophils and monocytes
D. Helper T cells and NK cells

back 62

D. Helper T cells and NK cells

front 63

A macrophage receives direct stimulation from bacterial lipopolysaccharide. What state can it enter?
A. Hyperactivated
B. Anergic
C. Tolerant
D. Naive

back 63

A. Hyperactivated

front 64

Lipopolysaccharide is classically associated with which bacteria?
A. Gram-positive bacteria
B. Acid-fast bacteria
C. Gram-negative bacteria
D. Intracellular protozoa

back 64

C. Gram-negative bacteria

front 65

A hyperactivated macrophage releases a cytokine that can kill tumor cells and virus-infected cells. Which cytokine is this?
A. IL-4
B. Histamine
C. TNF
D. IgG

back 65

C. TNF

front 66

TNF produced by hyperactivated macrophages can directly help kill which target?
A. Virus-infected cells
B. Resting macrophages
C. Red blood cells
D. Memory B cells

back 66

A. Virus-infected cells

front 67

Besides killing abnormal cells, TNF also helps perform which function?
A. Produce hemoglobin
B. Form neutrophil NETs
C. Block all cytokines
D. Activate immune cells

back 67

D. Activate immune cells

front 68

A hyperactivated macrophage increases intracellular organelles filled with destructive enzymes. Which organelles increase?
A. Ribosomes
B. Lysosomes
C. Peroxisomes
D. Nuclei

back 68

B. Lysosomes

front 69

A macrophage increases production of hydrogen peroxide during hyperactivation. This represents increased production of what?
A. Reactive oxygen molecules
B. Antibody constant regions
C. Class I MHCs
D. Selectin ligands

back 69

A. Reactive oxygen molecules

front 70

A macrophage encounters a parasite too large to ingest. Which hyperactivated ability helps attack it?
A. Antibody secretion
B. BCR expression
C. Lysosomal dumping
D. Hemoglobin release

back 70

C. Lysosomal dumping

front 71

Hyperactivated macrophages increase destructive potential through which change?
A. Fewer lysosomes
B. More lysosomes
C. Less TNF
D. Less ROS

back 71

B. More lysosomes

front 72

Hyperactivated macrophages can damage pathogens using which molecule?
A. Albumin
B. IgD
C. Hemoglobin
D. Hydrogen peroxide

back 72

D. Hydrogen peroxide

front 73

A neutrophil leaves bone marrow. On average, when will it die?
A. About 5 days
B. About 3 weeks
C. About 1 month
D. About 60 microseconds

back 73

A. About 5 days

front 74

Compared with macrophages, neutrophils are generally not which type of cell?
A. Phagocytes
B. Innate immune cells
C. Antigen-presenting cells
D. Short-lived cells

back 74

C. Antigen-presenting cells

front 75

Which cells uniquely liquefy tissues with destructive enzymes during infection?
A. Macrophages
B. Neutrophils
C. Plasma cells
D. Helper T cells

back 75

B. Neutrophils

front 76

A dying neutrophil releases web-like structures that trap bacteria and fungi. What are these called?
A. MHC complexes
B. Selectin ligands
C. NETs
D. Antibodies

back 76

C. NETs

front 77

NETs can trap or kill which organisms?
A. Bacteria only
B. Bacteria, viruses, fungi, parasites
C. Viruses only
D. Parasites only

back 77

B. Bacteria, viruses, fungi, parasites

front 78

Before infection, endothelial cells display which adhesion molecule?
A. Selectin ligand
B. ICAM
C. Integrin
D. C5a

back 78

B. ICAM

front 79

Neutrophils normally carry which surface molecule for rolling?
A. Selectin ligand
B. ICAM
C. TNF
D. MBL

back 79

A. Selectin ligand

front 80

During infection, nearby macrophages release which cytokines to activate endothelium?
A. IFN-gamma and IL-4
B. IL-10 and TGF-beta
C. IL-1 and TNF
D. IgG and IgM

back 80

C. IL-1 and TNF

front 81

IL-1 and TNF cause endothelial cells to produce which molecule?
A. Integrin
B. Selectin
C. C5a
D. f-met

back 81

B. Selectin

front 82

Selectin on endothelium binds which neutrophil molecule?
A. ICAM
B. Integrin
C. MHC II
D. Selectin ligand

back 82

D. Selectin ligand

front 83

Selectin binding to neutrophil selectin ligand causes what?
A. Neutrophil lysis
B. Antibody secretion
C. Neutrophil rolling
D. Class switching

back 83

C. Neutrophil rolling

front 84

While rolling, a neutrophil samples nearby tissue for which signals?
A. Inflammatory signals
B. Antibody chains
C. Hemoglobin fragments
D. Thymic hormones

back 84

A. Inflammatory signals

front 85

Which inflammatory signal can a rolling neutrophil detect?
A. IgD
B. C5a
C. Albumin
D. CD59

back 85

B. C5a

front 86

Which bacterial signal can help activate a rolling neutrophil?
A. IgA
B. C9
C. Hemoglobin
D. LPS

back 86

D. LPS

front 87

After sensing inflammatory signals, neutrophils push which protein to their surface?
A. Integrin
B. Selectin
C. MASP
D. C3a

back 87

A. Integrin

front 88

Neutrophil integrin binds which endothelial molecule?
A. Selectin ligand
B. MBL
C. ICAM
D. C9

back 88

C. ICAM

front 89

Integrin binding to ICAM causes which neutrophil behavior?
A. Faster rolling
B. Antibody release
C. Thymic exit
D. Full stopping

back 89

D. Full stopping

front 90

A neutrophil firmly adheres to endothelium after integrin-ICAM binding. What comes next?
A. MHC II loss
B. Tissue exit
C. IgG secretion
D. B-cell activation

back 90

B. Tissue exit

front 91

Which chemoattractant encourages stopped neutrophils to enter tissue?
A. C5a
B. IgE
C. CD59
D. Albumin

back 91

A. C5a

front 92

Bacterial protein fragments containing formyl methionine are also called what?
A. C5a peptides
B. LPS peptides
C. f-met peptides
D. MHC peptides

back 92

C. f-met peptides

front 93

f-met peptides help guide neutrophils toward which location?
A. Bone marrow
B. Thymus
C. Red pulp
D. Inflammation site

back 93

D. Inflammation site

front 94

In the neutrophil exit sequence, selectin mainly causes which event?
A. Firm adhesion
B. Rolling
C. Tissue liquefaction
D. NET release

back 94

B. Rolling

front 95

In the neutrophil exit sequence, integrin mainly causes which event?
A. Firm adhesion
B. Endothelial selectin production
C. C5 cleavage
D. Macrophage priming

back 95

A. Firm adhesion

front 96

A macrophage detects gram-negative LPS before major adaptive activation. Which receptor group enables detection?
A. B-cell receptors
B. Pattern-recognition receptors
C. Antibody constant regions
D. T-cell receptors only

back 96

B. Pattern-recognition receptors

front 97

Pattern-recognition receptors are used by immune cells to recognize what?
A. Invasion patterns
B. Hemoglobin variants
C. Antibody classes
D. Thymic hormones

back 97

A. Invasion patterns

front 98

Pattern-recognition receptors detect pathogen-associated molecular patterns, also called what?
A. DAMPs
B. NETs
C. PAMPs
D. MACs

back 98

C. PAMPs

front 99

Pattern-recognition receptors detect damage-associated molecular patterns, also called what?
A. NETs
B. PAMPs
C. MHCs
D. DAMPs

back 99

D. DAMPs

front 100

LPS from gram-negative bacteria is an example of what?
A. DAMP
B. PAMP
C. NET
D. MAC

back 100

B. PAMP

front 101

Intracellular molecules released after cell death are examples of what?
A. PAMPs
B. Antibodies
C. DAMPs
D. Selectins

back 101

C. DAMPs

front 102

Approximately how many receptor types are included among Pattern-recognition receptors?
A. Two
B. Five
C. Ten
D. Over twenty

back 102

D. Over twenty

front 103

Which PRR family is described as most studied?
A. Integrins
B. Toll-like receptors
C. Selectins
D. Immunoglobulins

back 103

B. Toll-like receptors

front 104

How many Toll-like receptors are described in this material?
A. Ten
B. Five
C. Three
D. Twenty

back 104

A. Ten

front 105

Which Toll-like receptor detects lipopolysaccharide?
A. TLR7
B. TLR9
C. TLR4
D. TLR3

back 105

C. TLR4

front 106

TLR4 is anchored in which location?
A. Phagolysosome
B. Plasma membrane
C. Nuclear membrane
D. Lysosome lumen

back 106

B. Plasma membrane

front 107

TLR4 points in which direction?
A. Inward
B. Outward
C. Nuclear
D. Cytosolic only

back 107

B. Outward

front 108

Which TLR detects viral single-stranded RNA?
A. TLR4
B. TLR9
C. TLR7
D. TLR2

back 108

C. TLR7

front 109

TLR7 detects ssRNA from viruses such as which examples?
A. Influenza and HIV-1
B. E. coli and Salmonella
C. HSV and bacteria
D. Staph and Strep

back 109

A. Influenza and HIV-1

front 110

Which TLR detects double-stranded DNA?
A. TLR4
B. TLR7
C. TLR2
D. TLR9

back 110

D. TLR9

front 111

TLR9 detects dsDNA from which sources?
A. Influenza and HIV-1
B. Bacteria and herpes simplex
C. Fungi and parasites
D. E. coli LPS only

back 111

B. Bacteria and herpes simplex

front 112

TLR7 and TLR9 are located on which structure?
A. Plasma membrane
B. Bone marrow cells
C. Phagolysosomes
D. Antibody surfaces

back 112

C. Phagolysosomes

front 113

TLR7 and TLR9 point in which direction?
A. Inward
B. Outward
C. Extracellular
D. Nuclear

back 113

A. Inward

front 114

Which molecule lets endothelium slow neutrophils during inflammation?
A. Integrin
B. Selectin
C. IFN-gamma
D. f-met

back 114

B. Selectin

front 115

A neutrophil exits blood by squeezing between endothelial cells. What drives this movement?
A. Hemoglobin binding
B. Antibody neutralization
C. Chemoattractant gradients
D. Class switching

back 115

C. Chemoattractant gradients

front 116

PRRs often recognize pathogen structures that cannot easily change. Why is this useful?
A. They are hidden intracellularly
B. They are pathogen-essential features
C. They are antibody-dependent targets
D. They are rapidly mutated

back 116

B. They are pathogen-essential features

front 117

A pathogen mutates a PRR-recognized structural feature and becomes nonviable. What does this demonstrate?
A. PRRs recognize optional features
B. PRRs require class I MHC
C. PRRs target essential structures
D. PRRs bind antibodies directly

back 117

C. PRRs target essential structures

front 118

The innate immune system’s primary defense against viruses is which system?
A. Complement system
B. Interferon system
C. Antibody system
D. Thymic system

back 118

B. Interferon system

front 119

A virally infected cell’s PRRs detect viral material. Which warning proteins are produced?
A. IFN-alpha and IFN-beta
B. TNF and IL-12
C. IL-2 and IL-4
D. C3 and factor B

back 119

A. IFN-alpha and IFN-beta

front 120

IFN-alpha and IFN-beta mainly interfere with which process?
A. Bacterial chemotaxis
B. Viral reproduction
C. Antibody class switching
D. Neutrophil rolling

back 120

B. Viral reproduction

front 121

IFN-alpha and IFN-beta are classified as which interferon type?
A. Type II
B. Type III
C. Type IV
D. Type I

back 121

D. Type I

front 122

IFN-gamma is classified as which interferon type?
A. Type I
B. Type II
C. Type III
D. Type IV

back 122

B. Type II

front 123

A cell binds IFN-alpha after nearby viral detection. What does it begin producing?
A. Antiviral proteins
B. Complement pores
C. B-cell receptors
D. Selectin ligands

back 123

A. Antiviral proteins

front 124

Type I interferons bind virus-infected cells and induce which response?
A. Antiviral protein production
B. Factor D cleavage
C. Antibody secretion
D. NET formation

back 124

A. Antiviral protein production

front 125

An uninfected cell binds interferon but has no viral attack. What happens initially?
A. Immediate apoptosis
B. Antibody secretion
C. Business as usual
D. Class II loss

back 125

C. Business as usual

front 126

An interferon-warned cell later becomes infected by virus. What is the expected outcome?
A. Proliferation
B. Apoptosis
C. Opsonization
D. Phagocytosis

back 126

B. Apoptosis

front 127

Many cells can produce type I interferon, but which WBC produces the most?
A. Neutrophil
B. Plasma B cell
C. Helper T cell
D. Plasmacytoid dendritic cell

back 127

D. Plasmacytoid dendritic cell

front 128

Plasmacytoid dendritic cells are especially important for producing which molecules?
A. IFN-alpha and IFN-beta
B. IgG and IgA
C. C5b and C9
D. IL-2 and histamine

back 128

A. IFN-alpha and IFN-beta

front 129

Natural killer cells defend against infections partly by producing what?
A. Cytokines
B. Antibodies
C. Hemoglobin
D. Selectins

back 129

A. Cytokines

front 130

Which cytokine can natural killer cells produce?
A. IL-4
B. IFN-gamma
C. IgM
D. C9

back 130

B. IFN-gamma

front 131

Besides cytokine production, NK cells defend by forcing target cells into what process?
A. Apoptosis
B. Opsonization
C. Neutralization
D. Class switching

back 131

A. Apoptosis

front 132

NK cells can inject suicide enzymes into target cells using which protein?
A. Perforin
B. Selectin
C. ICAM
D. MASP

back 132

A. Perforin

front 133

Perforin helps NK cells deliver which molecules?
A. Complement proteins
B. Suicide enzymes
C. Antibody chains
D. MHC molecules

back 133

B. Suicide enzymes

front 134

NK cells can also trigger apoptosis through which surface ligand?
A. Fas ligand
B. Selectin ligand
C. IL-2 ligand
D. C3b ligand

back 134

A. Fas ligand

front 135

Fas ligand on an NK cell binds which target-cell protein?
A. C3b
B. Fas
C. ICAM
D. MBL

back 135

B. Fas

front 136

Fas-Fas ligand interaction causes the target cell to do what?
A. Self-destruct
B. Present antibodies
C. Release hemoglobin
D. Produce C9

back 136

A. Self-destruct

front 137

NK cells differ from T cells because NK cells lack what?
A. Cytokines
B. T-cell receptors
C. Inhibitory receptors
D. Activating receptors

back 137

B. T-cell receptors

front 138

Instead of T-cell receptors, NK cells use which receptor types?
A. Activating and inhibitory
B. Heavy and light
C. Alpha and beta
D. Soluble and secreted

back 138

A. Activating and inhibitory

front 139

NK activating receptors motivate the cell to do what?
A. Not kill
B. Kill
C. Secrete antibody
D. Mature thymically

back 139

B. Kill

front 140

NK inhibitory receptors motivate the cell to do what?
A. Not kill
B. Kill immediately
C. Produce antibodies
D. Form MACs

back 140

A. Not kill

front 141

The NK “don’t kill” signal comes from recognition of which molecule?
A. Class II MHC
B. Class I MHC
C. IgG
D. C3bBb

back 141

B. Class I MHC

front 142

The NK “kill” signal comes from recognition of unusual surface what?
A. Hemoglobin fragments
B. Carbohydrates/proteins
C. Antibody constants
D. C9 pores

back 142

B. Carbohydrates/proteins

front 143

Unusual foreign carbohydrates or proteins suggest a cell is stressed by what?
A. Infection or cancer
B. Normal differentiation
C. Thymic maturation
D. Antibody secretion

back 143

A. Infection or cancer

front 144

A virus hijacks a host cell and stops class I MHC production. Which immune cell may miss it?
A. Neutrophil
B. Killer T cell
C. NK cell
D. Macrophage

back 144

B. Killer T cell

front 145

Why would a class I MHC-deficient infected cell evade killer T cells?
A. No class I display
B. Excess IFN-gamma
C. Too much C3b
D. More Fas ligand

back 145

A. No class I display

front 146

A class I MHC-deficient infected cell is placed near an NK cell. What happens?
A. NK ignores it completely
B. NK receives “don’t kill” signal
C. NK likely induces apoptosis
D. NK becomes a plasma cell

back 146

C. NK likely induces apoptosis

front 147

Why do NK cells kill cells with low class I MHC?
A. They detect antibodies
B. They lack inhibitory signal
C. They require BCR signaling
D. They bind class II MHC

back 147

B. They lack inhibitory signal

front 148

A cancerous cell has abnormal surface proteins but reduced class I MHC. Which immune cell is well suited to kill it?
A. NK cell
B. Plasma cell
C. Erythrocyte
D. Megakaryocyte

back 148

A. NK cell

front 149

In NK-macrophage cooperation, bacterial LPS first binds which cell?
A. Plasma cell
B. NK cell
C. Eosinophil
D. Basophil

back 149

B. NK cell

front 150

After LPS stimulation, NK cells produce which macrophage-priming cytokine?
A. IFN-gamma
B. IL-2
C. C3
D. CD59

back 150

A. IFN-gamma

front 151

IFN-gamma from NK cells does what to macrophages?
A. Primes macrophages
B. Destroys macrophages
C. Blocks TNF release
D. Prevents LPS binding

back 151

A. Primes macrophages

front 152

Primed macrophages can become hyperactivated by direct contact with what?
A. IgD
B. LPS
C. Hemoglobin
D. IL-2

back 152

B. LPS

front 153

A hyperactivated macrophage produces which cytokine in this feedback loop?
A. TNF
B. IgA
C. Perforin
D. C9

back 153

A. TNF

front 154

After producing TNF, the macrophage responds by secreting which cytokine?
A. IL-12
B. IL-2
C. IFN-beta
D. IgM

back 154

A. IL-12

front 155

IL-12 plus TNF influences NK cells to increase production of what?
A. IFN-gamma
B. C3b
C. Antibody
D. Hemoglobin

back 155

A. IFN-gamma

front 156

In the NK-macrophage loop, TNF increases NK-cell expression of which receptor?
A. IL-2 receptors
B. T-cell receptors
C. B-cell receptors
D. Class II receptors

back 156

A. IL-2 receptors

front 157

IL-2 acts as what for NK cells?
A. Growth factor
B. Opsonin
C. Anaphylatoxin
D. Convertase

back 157

A. Growth factor

front 158

IL-2 allows NK cells to do what?
A. Proliferate
B. Form antibodies
C. Express hemoglobin
D. Make C9 pores

back 158

A. Proliferate

front 159

In the NK-macrophage loop, which cytokine primes macrophages?
A. TNF
B. IFN-gamma
C. IL-2
D. IL-12

back 159

B. IFN-gamma

front 160

In the NK-macrophage loop, which cytokine helps induce IL-12 release?
A. TNF
B. IFN-alpha
C. IL-2
D. IgE

back 160

A. TNF

front 161

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back 161

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front 162

After IFN-gamma primes macrophages, what can LPS directly trigger?
A. Hyperactivation
B. Class I loss
C. Antibody switching
D. NET release

back 162

A. Hyperactivation

front 163

Which two cytokines together increase NK IFN-gamma output?
A. IL-12 and TNF
B. IL-2 and IFN-beta
C. IgG and IgA
D. C3a and C5a

back 163

A. IL-12 and TNF

front 164

Which cytokine causes NK cells to upregulate IL-2 receptors?
A. TNF
B. IFN-alpha
C. IFN-beta
D. IL-4

back 164

A. TNF

front 165

Activated macrophages can produce which complement protein?
A. C3
B. C9
C. C5a
D. CD59

back 165

A. C3

front 166

Activated macrophages can produce C3 and which factors?
A. Factors B and D
B. Factors H and I
C. Factors C and E
D. Factors A and C

back 166

A. Factors B and D

front 167

Complement proteins start being made during which fetal period?
A. First trimester
B. Second trimester
C. Third trimester
D. After birth

back 167

A. First trimester