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Summer Immuno Lecture 2

1.

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

B. Liver

2.

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

D. C3

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

A. C3a and C3b

4.

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

C. C3b

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

A. Amino or hydroxyl

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

D. 60 microseconds

7.

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

B. Water

8.

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

C. B

9.

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

A. D

10.

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

D. C3bBb

11.

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

B. Convertase

12.

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

C. C3

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

A. Positive feedback

14.

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

D. C3b

15.

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

B. C5

16.

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

A. C5a and C5b

17.

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

C. C5b

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

D. C6, C7, C8, C9

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

B. C5b, C6, C7, C8

20.

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

A. C9

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

C. Bacterial lysis

22.

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

D. Alternative pathway

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

A. B binds C3b

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

B. Cleaves bound B

25.

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

C. Cleaves C3

26.

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

D. Cleaves C5

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

A. C5b recruits C6-C9

28.

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

C. C3b

29.

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

B. MCP

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

D. Accelerates C3b inactivation

31.

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

A. DAF

32.

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

C. C3bBb destruction

33.

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

B. Protectin

34.

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

D. C9 attachment

35.

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

A. MBL

36.

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

C. Lectin

37.

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

B. MASP

38.

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

D. Mannose

39.

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

A. MASP

40.

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

C. C3

41.

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

D. Antibody

42.

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

B. Alternative pathway

43.

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

A. iC3b

44.

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

C. Inactive opsonin

45.

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

B. Opsonization

46.

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

D. C3b and C5b

47.

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

A. C3a and C5a

48.

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

C. Chemotaxis

49.

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

B. C5a

50.

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

D. Macrophages

51.

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

A. Anaphylatoxins

52.

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

C. Anaphylactic shock

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

D. Macrophages and neutrophils

54.

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

B. Macrophage

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

A. Below exposed tissue surfaces

56.

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

C. External environment

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

B. C3b is rapidly neutralized

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

C. Class II MHCs

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

A. Increased class II MHC

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

D. Macrophage priming

61.

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

B. IFN-gamma

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

D. Helper T cells and NK cells

63.

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

A. Hyperactivated

64.

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

C. Gram-negative bacteria

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

C. TNF

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

A. Virus-infected cells

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

D. Activate immune cells

68.

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

B. Lysosomes

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

A. Reactive oxygen molecules

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

C. Lysosomal dumping

71.

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

B. More lysosomes

72.

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

D. Hydrogen peroxide

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

A. About 5 days

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

C. Antigen-presenting cells

75.

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

B. Neutrophils

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

C. NETs

77.

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

B. Bacteria, viruses, fungi, parasites

78.

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

B. ICAM

79.

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

A. Selectin ligand

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

C. IL-1 and TNF

81.

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

B. Selectin

82.

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

D. Selectin ligand

83.

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

C. Neutrophil rolling

84.

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

A. Inflammatory signals

85.

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

B. C5a

86.

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

D. LPS

87.

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

A. Integrin

88.

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

C. ICAM

89.

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

D. Full stopping

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

B. Tissue exit

91.

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

A. C5a

92.

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

C. f-met peptides

93.

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

D. Inflammation site

94.

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

B. Rolling

95.

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

A. Firm adhesion

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

B. Pattern-recognition receptors

97.

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

A. Invasion patterns

98.

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

C. PAMPs

99.

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

D. DAMPs

100.

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

B. PAMP

101.

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

C. DAMPs

102.

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

D. Over twenty

103.

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

B. Toll-like receptors

104.

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

A. Ten

105.

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

C. TLR4

106.

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

B. Plasma membrane

107.

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

B. Outward

108.

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

C. TLR7

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

A. Influenza and HIV-1

110.

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

D. TLR9

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

B. Bacteria and herpes simplex

112.

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

C. Phagolysosomes

113.

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

A. Inward

114.

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

B. Selectin

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

C. Chemoattractant gradients

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

B. They are pathogen-essential features

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

C. PRRs target essential structures

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

B. Interferon system

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

A. IFN-alpha and IFN-beta

120.

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

B. Viral reproduction

121.

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

D. Type I

122.

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

B. Type II

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

A. Antiviral proteins

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

A. Antiviral protein production

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

C. Business as usual

126.

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

B. Apoptosis

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

D. Plasmacytoid dendritic cell

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

A. IFN-alpha and IFN-beta

129.

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

A. Cytokines

130.

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

B. IFN-gamma

131.

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

A. Apoptosis

132.

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

A. Perforin

133.

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

B. Suicide enzymes

134.

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

A. Fas ligand

135.

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

B. Fas

136.

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

A. Self-destruct

137.

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

B. T-cell receptors

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

A. Activating and inhibitory

139.

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

B. Kill

140.

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

A. Not kill

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

B. Class I MHC

142.

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

B. Carbohydrates/proteins

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

A. Infection or cancer

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

B. Killer T cell

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

A. No class I display

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

C. NK likely induces apoptosis

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

B. They lack inhibitory signal

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

A. NK cell

149.

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

B. NK cell

150.

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

A. IFN-gamma

151.

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

A. Primes macrophages

152.

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

B. LPS

153.

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

A. TNF

154.

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

A. IL-12

155.

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

A. IFN-gamma

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

A. IL-2 receptors

157.

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

A. Growth factor

158.

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

A. Proliferate

159.

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

B. IFN-gamma

160.

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

A. TNF

161.

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162.

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

A. Hyperactivation

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

A. IL-12 and TNF

164.

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

A. TNF

165.

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

A. C3

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

A. Factors B and D

167.

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

A. First trimester