Complement Activation Quiz

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Questions and Answers

What happens to C3b in the absence of an activating surface?

C3b cleaves Factor D

C3b is converted to iC3b (correct)

C3b forms a stable complex with C3a

C3b remains active and binds to Factor B

What role does Factor D play in the activation of C3b?

It inactivates C3b to iC3b

It enhances the deposition of C3b

It cleaves C3b to generate C3a

It cleaves Factor B to generate an active enzyme (correct)

What is the significance of C3bBb in the complement activation pathway?

It inhibits the spontaneous breakdown of C3

It converts iC3b back to active C3b

It directly binds to bacterial pathogens

It amplifies the deposition of C3b on surfaces (correct)

Which of the following statements about C3b is true?

C3b is inactivated unless bound to a bacterial surface Signup and view all the answers

How is C3b generated during spontaneous breakdown?

It occurs without an activating surface Signup and view all the answers

What is the primary role of the classical pathway in the complement system?

Activated by antibody binding Signup and view all the answers

Which of the following best describes the lectin pathway of complement activation?

An innate response influenced by mannose Signup and view all the answers

What molecule is primarily generated during complement activation that plays a critical role in opsonization?

C3b Signup and view all the answers

Which of the following pathways accounts for most complement activation?

Alternative pathway Signup and view all the answers

What is NOT an effect of complement activation?

Antibody production Signup and view all the answers

How does the alternative pathway initiate complement activation?

Via spontaneous activation during infection Signup and view all the answers

Which component is common to all three pathways of complement activation?

C3 Signup and view all the answers

What role do mast cells play in the context of complement activation?

They degranulate in response to inflammation Signup and view all the answers

What is the primary function of complement C3b in the immune response?

Opsonizes pathogens to enhance phagocytosis Signup and view all the answers

What are PAMPs, MAMPs, and DAMPs in the context of innate immunity?

Conserved molecular structures recognized by immune receptors Signup and view all the answers

Which of the following best describes the role of professional phagocytes?

They internalize pathogens through phagocytosis Signup and view all the answers

Why is it impractical for the immune system to encode responses to each potential pathogen?

Due to the vast diversity in potential pathogen shapes and sizes Signup and view all the answers

How are soluble factors in the immune system important for host defense?

They facilitate rapid detection and response to pathogens Signup and view all the answers

What determines the effectiveness of the innate immune system in recognizing a pathogen?

Specific receptors that bind to conserved molecular patterns Signup and view all the answers

Which of the following statements is true regarding complement proteins?

Complement proteins are present constitutively in the body fluids Signup and view all the answers

What commonly results from prolonged antibiotic treatment in the context of immune system recognition?

Enhanced susceptibility to diverse infections Signup and view all the answers

Which of the following is a function of Decay Accelerating Factor (DAF)?

Disassemble C3 convertase Signup and view all the answers

What is the primary role of Factor H and Factor I in the complement system?

Cleavage of C3b into an inactive form Signup and view all the answers

Which key effect does the complement C3 pathway NOT contribute to?

Cell apoptosis Signup and view all the answers

Which of the following categories do Toll-Like Receptors (TLRs) primarily fall under?

Pattern Recognition Receptors Signup and view all the answers

What is the result of ligand binding to Toll-Like Receptors?

Activation of antigen-presenting cells Signup and view all the answers

Which TLR is specifically activated by LPS (lipopolysaccharides)?

TLR4 Signup and view all the answers

Which signaling molecule is primarily associated with Toll-Like Receptor signaling pathways?

MyD-88 Signup and view all the answers

What type of cells are primarily activated as a result of TLR signaling?

Antigen-presenting cells Signup and view all the answers

Which of the following outcomes is NOT a shared result of complement C3 activation?

Direct cytotoxicity to pathogens Signup and view all the answers

Which types of molecules can activate the signaling pathways of Toll-Like Receptors?

A variety of microbial patterns Signup and view all the answers

What is the primary role of NFkB in the inflammation process?

To upregulate gene transcription of inflammatory cytokines Signup and view all the answers

Which step is necessary for the activation of IL-1 and IL-18 for secretion?

Proteolytic cleavage of pro-cytokines Signup and view all the answers

What type of molecules do Danger Associated Molecular Patterns (DAMPs) include?

Both extracellular and intracellular molecules associated with damage Signup and view all the answers

What initiates the gene transcription of inflammatory cytokines via TLRs?

Pathogen-associated molecular patterns Signup and view all the answers

What is caspase-1's role in the activation of IL-1 and IL-18?

It cleaves pro-cytokines to produce active forms Signup and view all the answers

Which of the following is NOT a consequence of PRR signaling?

Inhibition of inflammatory response Signup and view all the answers

What is the function of Caspase-11 in the context of PRR signaling?

It plays a role in activating inflammasomes Signup and view all the answers

In which cellular compartment are pro-cytokines like IL-1 and IL-18 initially located?

Cytoplasm Signup and view all the answers

What role do extracellular DAMPs play in inflammation?

They help activate immune cells Signup and view all the answers

What is a likely consequence of the release of active cytokines into the extracellular space?

Promotion of fibrinolysis Signup and view all the answers

What initiates the lectin pathway of complement activation?

Mannose-binding lectin binding to mannose Signup and view all the answers

Which enzyme is activated to cleave C2 and C4 in the lectin pathway?

MASP Signup and view all the answers

In the classical pathway, what is necessary for C1 activation?

IgM or IgG binding to bacteria Signup and view all the answers

What is formed when C4 and C2 are both cleaved in the complement activation pathway?

C4b2b complex Signup and view all the answers

How does C3b contribute to the complement system once bound to the surface?

Amplifies C3 cleavage Signup and view all the answers

Which component is crucial in the formation of the Membrane Attack Complex (MAC)?

C5b Signup and view all the answers

What role does C5a play in the complement system?

Promotes inflammation Signup and view all the answers

What type of cells are primarily involved in the process of phagocytosis during complement activation?

Neutrophils Signup and view all the answers

What is one of the purposes of opsonization in the complement system?

To enhance phagocytosis Signup and view all the answers

Which protein forms the terminal complement complex and is associated with cell lysis?

C9 Signup and view all the answers

What occurs after C5b aggregates with C6 and C7?

Assembly of the MAC Signup and view all the answers

In which stage is the C4b2b enzyme most actively involved?

Cleaving C2 and C4 Signup and view all the answers

Which function is NOT associated with complement activation?

Cell-mediated cytotoxicity Signup and view all the answers

What triggers the polymerization of C9 during the terminal pathway?

Formation of C5b678 Signup and view all the answers

Study Notes

Innate Immune Recognition

Innate immunity directly recognizes microbial infections through conserved molecular structures.
PAMPs, MAMPs, and DAMPs are defined as pathogen-associated molecular patterns, microbe-associated molecular patterns, and damage-associated molecular patterns, respectively.
Soluble factors like the complement system are important for activating and mediating host defense.
Major classes of pattern recognition receptors (PRRs) have specific functions and locations.
Professional phagocytes have receptors that bind pathogen surfaces, internalizing them through phagocytosis.
Pathogens are subsequently destroyed by multiple effector mechanisms within the phagolysosome.
The innate immune system rapidly recognizes pathogens, unlike adaptive immunity, which requires time and information to respond.

Clinical Correlate

A breeding colony of Brittany spaniels exhibited increased susceptibility to infections (sepsis, pneumonia, surgical site infections), primarily caused by Pseudomonas, E. coli, Clostridia, and Klebsiella.
Prolonged antibiotic treatments were required for recovery in the majority of dogs.

Learning Objectives

The innate immune system directly recognizes microbial infection through conserved molecular structures.
PAMPs, MAMPs, and DAMPs.
Soluble factors play critical roles in activating and mediating host defense.
Major classes of pattern recognition receptors, their functions, and locations.

Layers of Host Protection

Anatomical barriers (skin, oral mucosa, respiratory epithelium, and intestine).
Complement/antimicrobial proteins (C3, defensins, RegIII).
Innate immune cells (macrophages, granulocytes, natural killer cells, epithelial cells).
Adaptive immunity (B cells, antibodies, and T cells).

The Complement System

Complement proteins are constitutively present in blood and interstitial spaces.
Complement protein C3 is crucial within the complement cascade.
C3 is cleaved into C3a and C3b.
C3b covalently binds to bacterial surfaces, acting as an opsonin, enhancing phagocytosis.
The complement system can be activated via the alternative, lectin, or classical pathways.
Complement activation leads to altered membranes, bacterial lysis, opsonization, phagocytosis, mast cell degranulation, neutrophil chemotaxis, inflammation, immune regulation, angiogenesis, and removal of apoptotic cells.

Three Ways to Activate Complement

Alternative pathway: an innate pathway, common in complement activation
Lectin pathway: another innate pathway triggered by mannose on microbial surfaces.
Classical pathway: triggered by antibody binding, part of the adaptive response.

Complement Pathway Outcomes

Membrane attack complex (MAC) formation: leads to cell lysis.
Opsonization: enhances phagocytosis.
Inflammation: associated with complement activation.

Why Host Cells Aren't Lysed

Host cells have protective complement control proteins, like decay-accelerating factor (DAF), which prevent the complement cascade from attacking host cells.

Three Shared Outcomes of Complement C3

Opsonization: Enhancement of phagocytosis by complement components.
Inflammation: Complement activation facilitates inflammation at the site of infection.
Cell lysis: via the formation of the membrane attack complex (MAC).

Pattern Recognition Receptors (PRRs)

Toll-like receptors (TLRs): innate signaling receptors recognizing pathogen-associated patterns.
TLR ligands: variety of patterns present in microbes (e.g., LPS, DNA, RNA, flagellin).
TLR function: activate antigen-presenting cells, induce inflammatory cytokines (TNF, IL-1), induce antiviral cytokines, and induce phagocytosis and killing.

Toll-like Receptor Signaling and Outcomes

Ligand binding to TLR activates intracellular signaling pathways leading to NF-κB activation.
NF-κB upregulates the expression of inflammatory cytokines (e.g., TNF, IL-1, IL-6), involved in the host response.

IL-1 and IL-18 Secretion

These cytokines require a secondary step involving inflammasomes and caspase cleavage for secretion.

Danger-Associated Molecular Patterns (DAMPs)

DAMPs are products of damaged host cells or from intracellular components released upon cellular damage.
DAMPs activate immune signaling pathways similar to pathogen-associated molecular patterns (PAMPs), triggering inflammation at the site of injury or infection.
DAMPs include mitochondrial DNA, uric acid, chromatin, heat shock proteins, adenosine, galectins, S100 proteins, cathelicidins, defensins, N-formyl peptides, and lactoferrin.

Consequences of PRR Signaling

Inflammation: cytokines cause blood vessel permeability, enabling effector cells and fluid containing soluble effector molecules to enter the infected tissue.
Recruit immune cells: cytokines like chemokines direct neutrophils, macrophages, and other immune cells to the site of infection.
Increase body temperature at the infection sites(induced by cytokines): enhances immune response.

Summary

Soluble factors enhance cell recruitment, tagging microbes for phagocytosis or direct killing.
The complement cascade covalently attaches C3b, acting as an opsonin.
Soluble PRRs mark microbes and enhance phagocytosis.
Membrane-bound PRRs activate cells and induce cytokine production, also directly contributing to phagocytosis.
PRR activation results in cytokine secretion, affecting both local and system-wide responses.

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Description

Test your knowledge on the complement activation pathways, including the classical, alternative, and lectin pathways. This quiz covers crucial components such as C3b, Factor D, and the significance of C3bBb. Evaluate your understanding of the effects and roles of complement system elements.