Chapter 3: Complement System

Q1. What is the complement system made of? a) Over 30 different proteins in blood plasma b) A single protein in the blood c) Cells in the bone marrow d) Antibodies produced by B cells

a

Q2. The complement system works through a cascade of what type of reactions? a) Oxidation reactions b) Proteolytic cleavage reactions c) Phosphorylation reactions d) Hydrolysis reactions

b

Q3. What are the two main functions of the complement system? a) Produce antibodies and kill viruses b) Tag pathogens for phagocytosis (opsonin) and directly kill pathogens by creating holes in their membranes (MAC) c) Activate T cells and B cells d) Produce cytokines and chemokines

b

Q4. What does MAC stand for? a) Macrophage Activation Complex b) Membrane Attack Complex c) Major Antibody Complex d) Microbial Adhesion Complex

b

Q5. What is the key complement protein that all pathways converge on? a) C1 b) C2 c) C3 d) C5

c

Q6. C3 is cleaved to form which two fragments? a) C3a and C3b b) C3a and C3c c) C3b and C3c d) C3d and C3b

a

Q7. What is the function of C3a? a) Opsonin that tags pathogens b) Anaphylatoxin that induces inflammation, recruits phagocytes, and induces degranulation c) Forms the membrane attack complex d) Cleaves C5

b

Q8. What is the function of C3b? a) Anaphylatoxin that induces inflammation b) Opsonin that covalently attaches to pathogen surface to induce phagocytosis c) Forms the membrane attack complex d) Cleaves C2

b

Q9. How does C3b attach to the pathogen surface? a) Via a newly exposed reactive thioester group b) Via an antibody c) Via a receptor d) Via a carbohydrate

a

Q10. What enzyme cleaves C3 into C3a and C3b? a) C3 convertase b) C5 convertase c) Factor D d) Factor B

a

Q11. What is the smaller fragment of C3 called? a) C3b b) C3a c) iC3b d) C3c

b

Q12. What is the larger fragment of C3 called? a) C3a b) C3b c) iC3b d) C3c

b

Q13. Where is C3 always present? a) In the blood plasma b) In the bone marrow c) In the lymph nodes d) In the spleen

a

Q14. What are the three pathways of complement activation? a) Alternative, lectin, classical b) Innate, adaptive, memory c) Primary, secondary, tertiary d) Direct, indirect, mixed

a

Q15. Which pathway is spontaneous and already initiated and ready to go whenever a pathogen enters the body? a) Lectin pathway b) Classical pathway c) Alternative pathway d) All of the above

c

Q16. Which pathway is activated by recognition of bacterial oligosaccharides ending in mannose or fucose? a) Alternative pathway b) Lectin pathway c) Classical pathway d) None of the above

b

Q17. Which pathway is best activated by antibodies bound to pathogen surface? a) Alternative pathway b) Lectin pathway c) Classical pathway d) All of the above

c

Q18. What is the order of action for the three pathways (first to act to last)? a) Classical → Lectin → Alternative b) Alternative → Lectin → Classical c) Lectin → Classical → Alternative d) Alternative → Classical → Lectin

b

Q19. All three pathways converge on the formation of what? a) C3 convertase b) C5 convertase c) Membrane attack complex d) C1 complex

a

Q20. What is the C3 convertase of the alternative pathway? a) C4bC2b b) C3bBb c) C3b₂Bb d) C4bC2bC3b

b

Q21. What is the C3 convertase of the lectin and classical pathways? a) C3bBb b) C4bC2b c) C3b₂Bb d) C1qC1rC1s

b

Q22. Which pathway functions in the absence of infection? a) Lectin pathway b) Classical pathway c) Alternative pathway d) All of the above

c

Q23. Do the lectin and classical pathways produce the same C3 convertase? a) Yes, both produce C4bC2b b) No, lectin produces C3bBb and classical produces C4bC2b c) No, lectin produces C4bC2b and classical produces C3bBb d) Yes, both produce C3bBb

a

Q24. Which pathway is first to act? a) Classical b) Lectin c) Alternative d) All act at the same time

c

Q25. Which pathway is second to act? a) Classical b) Lectin c) Alternative d) None of the above

b

Q26. Which pathway is third to act? a) Classical b) Lectin c) Alternative d) None of the above

a

Q27. What happens to C3 in the alternative pathway's first step? a) C3 is cleaved by C1 b) C3 spontaneously hydrolyzes to iC3 c) C3 binds to antibodies d) C3 is cleaved by MASP-2

b

Q28. What binds to iC3 in the alternative pathway? a) Factor D b) Factor B c) Factor H d) Properdin

b

Q29. What cleaves Factor B in the alternative pathway? a) Factor B b) Factor D c) Factor H d) Factor I

b

Q30. What is the alternative pathway C3 convertase? a) C4bC2b b) C3bBb c) iC3Bb d) C3b₂Bb

b

Q31. What is the function of Properdin (Factor P)? a) Brake — destabilizes C3bBb on host cells b) Accelerator — stabilizes C3bBb on pathogen surfaces c) Cleaves C3b d) Binds to sialic acid

b

Q32. What is the function of Factor H? a) Accelerator — stabilizes C3bBb on pathogen surfaces b) Brake — binds to C3b and promotes cleavage by Factor I to form inactive iC3b c) Cleaves Factor B d) Forms the MAC

b

Q33. Where does Factor H preferentially bind? a) Pathogen cell membranes b) Host cell membranes via interaction with sialic acid c) C3b on any surface d) Factor B

b

Q34. What is the function of Decay Accelerating Factor (DAF)? a) Stabilizes C3bBb on pathogen surfaces b) Inactivates C3bBb by promoting dissociation of Bb from C3b c) Cleaves C3b d) Binds to sialic acid

b

Q35. What is the function of Membrane Cofactor Protein (MCP)? a) Stabilizes C3bBb on pathogen surfaces b) Binds to C3bBb and promotes both dissociation of Bb and cleavage of remaining C3b by Factor I c) Cleaves Factor B d) Forms the MAC

b

Q36. What are the two families of regulatory proteins that control complement activation? a) Plasma proteins and membrane proteins b) Cytoplasmic proteins and nuclear proteins c) Intracellular proteins and extracellular proteins d) Soluble proteins and insoluble proteins

a

Q37. What is the positive feedback loop of the alternative pathway? a) C3bBb cleaves more C3 → more C3b → more C3bBb b) C3a cleaves more C3 c) Factor H cleaves more C3b d) Properdin cleaves more Factor B

a

Q38. What is the role of Factor I? a) Cleaves C3b to form inactive iC3b (with help from Factor H, MCP) b) Stabilizes C3bBb c) Cleaves Factor B d) Forms the MAC

a

Q39. What is the role of sialic acid in complement regulation? a) It helps Factor H bind to host cells, protecting them b) It helps Factor H bind to pathogens, destroying them c) It activates the classical pathway d) It forms the MAC

a

Q40. What does C3b bind to make alternative C3 convertase? a) Factor B b) Factor D c) Factor H d) Properdin

a

Q41. What is the function of C3b in the alternative pathway? a) Binds Factor B to form C3bBb (alternative C3 convertase) b) Cleaves C5 c) Forms the MAC d) Is an anaphylatoxin

a

Q42. What is the alternative C5 convertase? a) C3bBb b) C3b₂Bb c) C4bC2b d) C4bC2bC3b

b

Q43. What does C5 convertase cleave C5 into? a) C5a and C5b b) C5b and C5c c) C5a and C5c d) C5d and C5b

a

Q44. What is the function of C5a? a) Opsonin b) Anaphylatoxin c) Forms the MAC d) Cleaves C3

b

Q45. What is the function of C5b? a) Opsonin b) Anaphylatoxin c) Initiates formation of the membrane-attack complex by interacting with C6 and C7 d) Cleaves C3

c

Q46. What does C5b associate with to form the C5b67 complex? a) C3 and C4 b) C6 and C7 c) C8 and C9 d) C1 and C2

b

Q47. What allows C5b67 to associate with the pathogen membrane? a) Hydrophilic region of C7 b) Hydrophobic region of C7 c) Thioester bond of C7 d) Carbohydrate of C7

b

Q48. What does C8 do in MAC formation? a) Binds C5b67 to serve as a docking site for C9 b) Forms transmembrane pores c) Cleaves C5 d) Stabilizes C3bBb

a

Q49. What does C9 do in MAC formation? a) Binds C8 and forms transmembrane pores in pathogen surfaces b) Cleaves C5 c) Stabilizes C3bBb d) Binds C5b67

a

Q50. What is the function of the membrane attack complex? a) Opsonize pathogens b) Create holes in pathogen membranes → lysis c) Induce inflammation d) Recruit phagocytes

b

Q51. What plasma proteins inhibit recruitment of C6 and C7 to C5b? a) Properdin, Factor H, Factor I b) S protein, clusterin, factor J c) DAF, MCP, CD59 d) C1-inh, C4bp, Factor I

b

Q52. What membrane proteins on host cells inhibit C9 polymerization? a) DAF and MCP b) Protectin (CD59) and Homologous restriction factor (HRF) c) Factor H and Factor I d) Properdin and Factor P

b

Q53. What is the correct order of MAC formation? a) C5b → C6 → C7 → C8 → C9 b) C5a → C6 → C7 → C8 → C9 c) C5b → C7 → C6 → C8 → C9 d) C5b → C6 → C8 → C7 → C9

a

Q54. What is the role of C5b67 in MAC formation? a) Inserts into pathogen membrane via hydrophobic region of C7 b) Cleaves C5 c) Opsonizes pathogens d) Is an anaphylatoxin

a

Q55. What does C8 do in MAC formation? a) Nucleates polymerization of C9 molecules b) Cleaves C5 c) Opsonizes pathogens d) Is an anaphylatoxin

a

Q56. What are C3a and C5a? a) Opsonins b) Anaphylatoxins c) Convertases d) MAC components

b

Q57. What do C3a and C5a do? a) Bind to endothelial cells to increase vascular permeability b) Induce degranulation of mast cells and basophils c) Act as chemoattractants for phagocytes d) All of the above

d

Q58. What else do C3a and C5a do to phagocytes? a) Decrease expression of complement receptors b) Increase expression of complement receptors c) Kill phagocytes d) Prevent phagocytosis

b

Q59. Where do C3a and C5a bind? a) Endothelial cells b) Pathogen surfaces c) C3 convertase d) Factor B

a

Q60. What do C3a and C5a induce in mast cells and basophils? a) Apoptosis b) Degranulation c) Proliferation d) Phagocytosis

b

Q61. What do C3a and C5a bind to on endothelial cells? a) C3a receptor or C5a receptor b) TLR4 c) CR3 d) Fc receptor

a

Q62. What do C3a and C5a act as for phagocytes? a) Chemoattractants b) Opsonins c) Convertases d) MAC components

a

Q63. What do C3a and C5a increase on phagocytes? a) Expression of complement receptors b) Expression of TLRs c) Expression of antibodies d) Expression of MHC

a

Q64. Where are lectin and classical pathway initiator proteins produced? a) Bone marrow b) Liver cells in response to inflammatory cytokines c) Spleen d) Lymph nodes

b

Q65. What does Mannose-binding lectin (MBL) bind to? a) Antibodies b) Mannose on pathogen cell surfaces c) Phosphocholine d) Sialic acid

b

Q66. What proteases are complexed with MBL? a) C1r and C1s b) MASP-1 and MASP-2 c) Factor B and Factor D d) Factor H and Factor I

b

Q67. What does C-reactive protein (CRP) bind to? a) Mannose b) Phosphocholine on pathogen cell surfaces c) Sialic acid d) Antibodies

b

Q68. What does C-reactive protein on pathogen surface bind? a) MBL b) C1q hexamer complexed with proteases C1r and C1s c) Factor B d) Properdin

b

Q69. Do both MBL and C-reactive protein act as opsonins? a) Yes b) No, only MBL c) No, only CRP d) No, neither

a

Q70. What receptors do monocytes and macrophages have for? a) MBL and C-reactive protein b) C3a and C5a c) Factor B and Factor D d) Properdin and Factor H

a

Q71. What do activated MASP-1 and MASP-2 (lectin pathway) or C1r and C1s (classical pathway) cleave? a) C3 into C3a and C3b b) C4 into C4a and C4b; C2 into C2a and C2b c) C5 into C5a and C5b d) Factor B into Ba and Bb

b

Q72. What forms the classical C3 convertase? a) C3bBb b) C4bC2b c) C3b₂Bb d) C1qC1rC1s

b

Q73. How does C4b attach to the cell surface? a) Via a thioester bond (like C3b) b) Via an antibody c) Via a receptor d) Via a carbohydrate

a

Q74. What is the role of C-reactive protein (CRP)? a) Binds phosphocholine on pathogens; acts as opsonin; initiates classical pathway b) Binds mannose on pathogens; initiates lectin pathway c) Cleaves C3 d) Forms the MAC

a

Q75. What is the role of Mannose-binding lectin (MBL)? a) Binds phosphocholine on pathogens; initiates classical pathway b) Binds mannose on pathogens; acts as opsonin; initiates lectin pathway c) Cleaves C3 d) Forms the MAC

b

Q76. What do MBL and C-reactive protein initiate? a) Parallel and homologous pathways to form the classical C3 convertase b) The alternative pathway only c) The MAC directly d) Antibody production

a

Q77. What connects activation of innate immune cells to complement activation? a) The acute-phase response b) The inflammatory response c) The adaptive immune response d) The coagulation system

a

Q78. What do macrophages secrete in response to PRR activation? a) Antibodies b) Inflammatory cytokines c) Complement proteins d) Defensins

b

Q79. What does IL-6 act on to induce production of acute-phase proteins? a) Bone marrow b) Liver cells c) Spleen d) Lymph nodes

b

Q80. What acute-phase proteins are produced by the liver? a) C-reactive protein and MBL b) C3 and C5 c) Factor B and Factor D d) Properdin and Factor H

a

Q81. Activation of lectin and classical pathways produce what? a) Alternative C3 convertase b) Classical C3 convertase and C3b c) C5 convertase d) MAC

b

Q82. What can C3b bind to make alternative C3 convertase? a) Factor B b) Factor D c) Factor H d) Properdin

a

Q83. What is the correct sequence of the acute-phase response? a) Macrophage detects pathogen → IL-6 → liver makes CRP/MBL → complement activated b) Liver makes CRP → macrophage detects pathogen → IL-6 → complement activated c) Complement activated → macrophage detects pathogen → IL-6 → liver makes CRP d) IL-6 → macrophage detects pathogen → liver makes CRP → complement activated

a

Q84. What does the blood coagulation system do? a) Minimizes blood loss b) Hinders entry of pathogens into blood circulation c) Platelets release prostaglandin and other factors to boost innate immune response d) All of the above

d

Q85. What does bradykinin do? a) Causes vasodilation and attracts innate immune cells b) Cleaves C3 c) Forms the MAC d) Opsonizes pathogens

a

Q86. What percentage of plasma proteins are protease inhibitors? a) 1% b) 5% c) 10% d) 25%

c

Q87. What does α2-macroglobulin do? a) Cleaves C3 b) Traps proteases — protease attack exposes internal thioester that bonds with protease; shape change encloses protease c) Forms the MAC d) Opsonizes pathogens

b

Q88. What are defensins? a) Large proteins b) Small (35-40 amino acids) amphipathic peptides c) Carbohydrates d) Lipids

b

Q89. Where are α-defensins made? a) Neutrophils and Paneth cells of small intestine b) Epithelial cells c) Liver cells d) Bone marrow

a

Q90. Where are β-defensins made? a) Neutrophils b) Various types of epithelial cells c) Liver cells d) Bone marrow

b

Q91. What is true about defensins evolutionarily? a) They are the newest immune defense mechanisms b) They are among the oldest immune defense mechanisms c) They only exist in humans d) They are not found in other animals

b

Q92. What do platelets release to boost innate immune response? a) Prostaglandin and other factors b) Antibodies c) Complement proteins d) Defensins

a

Q93. What does the blood coagulation system minimize? a) Blood loss b) Pathogen entry c) Inflammation d) Complement activation

a

Q94. What do defensins do to microbial membranes? a) Insert into membranes → form pores → pathogen leaks and dies b) Strengthen membranes c) Opsonize pathogens d) Cleave C3

a

Q95. What happens when there is a deficiency in complement? a) Abnormal clearance of Gram-positive bacteria b) Difficulty removing immune complexes c) Recurring bacterial infections d) All of the above

d

Q96. Why is clearance of Gram-positive bacteria abnormal in complement deficiency? a) PAMPs are masked from PRRs of innate immune cells; opsonization by complement facilitates clearance by phagocytes b) Antibodies are not produced c) T cells cannot recognize bacteria d) Macrophages are not produced

a

Q97. What can accumulation of soluble immune complexes lead to? a) Hypersensitivity reactions and autoimmunity b) Increased bacterial clearance c) Enhanced MAC formation d) Increased opsonization

a

Q98. Deficiency in which complement protein causes Systemic lupus erythematosus and Rheumatoid arthritis? a) C3 b) C1 c) C9 d) Factor B

b

Q99. Deficiency in which complement protein causes Hereditary angioedema? a) C1-inhibitor (C1-inh) b) C3 c) C9 d) Properdin

a

Q100. Deficiency in which complement protein causes recurring bacterial infections and Systemic lupus erythematosus? a) C1 b) C2 c) C3 d) C4

b