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Questions and Answers
Which of the following statements accurately describes the mechanism by which complement contributes to bacterial lysis?
Which of the following statements accurately describes the mechanism by which complement contributes to bacterial lysis?
- The C5 convertase cleaves C5 into C5a and C5b, with C5b initiating MAC assembly, leading to pore formation in the bacterial membrane. (correct)
- C3b, after binding to bacterial surfaces, activates the C5 convertase, which then directly lyses the bacteria.
- C3a directly binds to bacterial cell walls, creating pores that allow the entry of antimicrobial enzymes.
- Complement proteins directly bind to bacterial DNA, disrupting its structure and leading to bacterial cell death.
What is the primary function of C3b in the complement cascade?
What is the primary function of C3b in the complement cascade?
- Serve as an opsonin, tagging bacteria for phagocytosis by immune cells. (correct)
- Activate the C5 convertase, leading to the release of C5a, a potent chemoattractant.
- Directly lyse bacterial cells by creating pores in their membranes.
- Recruit and activate leukocytes by binding to specific receptors on their surface.
How does CD59 protect mammalian cells from complement-mediated lysis?
How does CD59 protect mammalian cells from complement-mediated lysis?
- CD59 directly inactivates the C5 convertase, preventing the formation of C5b.
- CD59 stimulates the release of anti-inflammatory cytokines, reducing the inflammatory response triggered by complement.
- CD59 blocks the assembly of the C5b-C8 complex, inhibiting the recruitment of C9 and the formation of the MAC. (correct)
- CD59 binds to C3b, preventing its attachment to mammalian cells.
Which of the following statements accurately describes the role of anaphylatoxins in the complement cascade?
Which of the following statements accurately describes the role of anaphylatoxins in the complement cascade?
Why are individuals with terminal complement deficiency susceptible to recurrent infections?
Why are individuals with terminal complement deficiency susceptible to recurrent infections?
What is the function of the C1q component in the classical pathway of complement activation?
What is the function of the C1q component in the classical pathway of complement activation?
How does the alternative pathway of complement activation differ from the classical and lectin pathways?
How does the alternative pathway of complement activation differ from the classical and lectin pathways?
Which of these components is NOT directly involved in the formation of the classical C3 convertase?
Which of these components is NOT directly involved in the formation of the classical C3 convertase?
What is the role of MASP2 in the lectin pathway?
What is the role of MASP2 in the lectin pathway?
How does the formation of the C5 convertase in the alternative pathway differ from that in the classical and lectin pathways?
How does the formation of the C5 convertase in the alternative pathway differ from that in the classical and lectin pathways?
What is the function of the membrane attack complex (MAC) in the complement system?
What is the function of the membrane attack complex (MAC) in the complement system?
Which of the following statements is TRUE regarding the complement system's role in inflammation?
Which of the following statements is TRUE regarding the complement system's role in inflammation?
Which complement component is involved in both the classical and lectin pathways?
Which complement component is involved in both the classical and lectin pathways?
Flashcards
Complement System
Complement System
Part of the innate immune system that helps eliminate pathogens.
C3 Convertase
C3 Convertase
An enzyme complex that cleaves C3 into C3a and C3b, critical for complement activity.
Classical Pathway
Classical Pathway
A complement activation pathway starting with antibody binding, leading to C3 convertase formation.
Lectin Pathway
Lectin Pathway
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Alternative Pathway
Alternative Pathway
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C5 Convertase
C5 Convertase
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Opsonization
Opsonization
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Membrane Attack Complex (MAC)
Membrane Attack Complex (MAC)
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C3b Function
C3b Function
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Anaphylatoxin
Anaphylatoxin
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Complement Regulation
Complement Regulation
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Study Notes
The Complement System
- Part of the innate immune system, found in blood plasma, produced in the liver
- Key roles: cell lysis, opsonization (tagging), proinflammatory signaling and chemoattraction
Complement Pathways
- All pathways converge to form C3 convertase and the membrane attack complex (MAC)
- Classical Pathway:
- Initiated by antibody binding to pathogen
- C1 complex (C1q, C1r, C1s) binds to antibody Fc region
- C1r cleaves C1s, triggering a cascade cleaving C4 and C2
- C4b binds to pathogen, then binds C2, creating C4bC2a (classical C3 convertase)
- The convertase can also directly bind to bacterial surfaces
- Lectin Pathway:
- Initiated by mannose-binding lectin (MBL) binding to mannose on pathogen surfaces
- MBL-associated serine proteases (MASP) cleave C4 and C2
- Resulting in C4b and C2a forming C4bC2a (lectin C3 convertase)
- Alternative Pathway:
- Does not require antibody or prior microbe activation
- C3 (in the blood) is hydrolyzed to C3(H2O)
- C3(H2O) binds Factor B, then Factor D cleaves Factor B into Bb and Ba
- Bb binds C3(H2O) to form C3(H2O)Bb (initial C3 convertase)
- C3b binds to microbial surface, creating C3 convertase amplifier loop
Terminal Complement Pathway
- C5 convertase formation:
- Alternative pathway: C3bBb binds another C3b to make C3bBbC3b (C5 convertase)
- Lectin/classical pathway: C4b2a binds another C3b to make C4b2aC3b (C5 convertase)
- C5 cleavage: C5 convertase cleaves C5 into C5a and C5b
- MAC formation:
- C5b initiates the assembly of the MAC
- C6, C7, and C8 are recruited to the membrane
- C9 polymerization forms a pore in the pathogen membrane
- This leads to bacterial lysis and cell death
Complement Function Summary
- Opsonization: C3b and C4b covalently attach to microbes, marking them for the immune system (like a flag)
- Inflammation: Cleaved fragments (e.g., C3a and C5a) activate immune cells and cause inflammation at the infection site
- Lysis (membrane attack): The MAC creates holes in bacterial membranes.
Complement Regulation (Avoidance of Attacking Self-Cells)
- Cells have molecules that inhibit complement activation, preventing attack on healthy cells (e.g., CD59 on human cells).
- Deficiency in terminal complement components can lead to increased susceptibility to infections.
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