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inmuno > cytokine_questions_complete_final_v4 > Flashcards

cytokine_questions_complete_final_v4 Flashcards

1
Q

What are the six families of cytokines?

A

IL-1, Class I cytokines (hematopoietin), Class II cytokines (interferon), TNF family, IL-17 family, Chemokines

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2
Q

What is the representative member of the IL-1 cytokine family?

A

IL-1α, IL-1β, IL-1Ra, IL-18, IL-33

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3
Q

Name one cytokine from the Class I cytokine family (hematopoietin).

A

IL-2, IL-3, IL-4, IL-5

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4
Q

Which cytokine family does Interferon (IFN) belong to?

A

Class II cytokines

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5
Q

What are the representative members of the IL-17 family?

A

IL-17A, IL-17B, IL-17C, IL-17D, IL-17F

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6
Q

What family do chemokines belong to?

A

Chemokines

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7
Q

Which cytokine is a member of both IL-1 and TNF family?

A

IL-1β

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8
Q

What is the role of IL-1 in cytokine signaling?

A

Initiates inflammatory response

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9
Q

Name a cytokine involved in growth hormone signaling.

A

Insulin-like Growth Factor 1 (IGF-1)

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10
Q

Which family of cytokines is associated with hematopoiesis?

A

Class I cytokines (hematopoietin)

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11
Q

What function do TNF family cytokines have?

A

Involved in cell death and survival signaling

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12
Q

Which family includes cytokines involved in the antiviral response?

A

Class II cytokines (interferon)

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13
Q

Name a cytokine that is part of the chemokine family.

A

IL-8, CCL19, CCL21, RANTES

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14
Q

What cytokine is part of the inflammatory response and also involved in fever production?

A

IL-1β

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15
Q

Which cytokine is involved in the immune response and is a key player in autoimmune diseases?

A

IL-17

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16
Q

What is the function of chemokines in immune cell trafficking?

A

Direct the movement of immune cells to sites of infection or inflammation

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17
Q

Which cytokine is a major player in tumor necrosis?

A

TNF-α

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18
Q

What is a key function of interferons (IFN)?

A

Inhibit viral replication and modulate the immune response

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19
Q

What cytokine is critical in the adaptive immune response?

A

IL-2

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20
Q

Which cytokine is important in the activation of macrophages?

A

IFN-γ

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21
Q

Which cytokine family includes cytokines important for the differentiation of immune cells?

A

Class I cytokines (hematopoietin)

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22
Q

Which cytokine promotes the survival of T cells?

A

IL-2

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23
Q

Name a cytokine that stimulates the production of antibodies.

A

IL-4

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24
Q

What role does IL-17 play in chronic inflammation?

A

Promotes the recruitment of neutrophils to sites of inflammation

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25
Q

Which cytokine family is known for regulating immune cell communication?

A

Chemokines

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26
Q

What cytokine is important in allergic responses?

A

IL-4

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27
Q

What is the key role of TNF-α in inflammation?

A

Induces the inflammatory response and regulates immune cells

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28
Q

What cytokine helps in the regulation of hematopoietic stem cells?

A

IL-3

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29
Q

Which cytokine is involved in both immunity and neural development?

A

IL-6

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30
Q

What are the main functions of cytokines in the IL-1 family?

A

Inducing primarily proinflammatory responses.

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31
Q

Name a cytokine from the Class I cytokine (hematopoietin) family.

A

IL-2, IL-4, IL-6, EPO (erythropoietin), GM-CSF

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32
Q

What is the primary function of Class I cytokines (hematopoietin)?

A

Regulation of hematopoiesis and immune function.

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33
Q

What receptor type do IL-1 family cytokines interact with?

A

Dimeric receptors.

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34
Q

What are interferons and which cytokine family do they belong to?

A

Interferons (IFN-α, IFN-β, IFN-γ) belong to the Class II cytokine family (interferon).

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35
Q

What is the role of Type I interferons (IFN-α and IFN-β)?

A

Mediating early antiviral responses.

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36
Q

What is the function of Type II interferons (like IFN-γ)?

A

Activating macrophages and supporting adaptive immunity.

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37
Q

Name a cytokine from the TNF family.

A

TNF-α, TNF-β, FasL, CD40L

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38
Q

How do TNF family cytokines typically interact with their receptors?

A

They act as trimers and can appear in soluble or membrane-bound forms.

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39
Q

What are the main functions of TNF family cytokines?

A

Inducing differentiation, survival, proliferation, and apoptosis.

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40
Q

What are the key characteristics of the IL-17 cytokine family?

A

Members are proinflammatory in action, promoting neutrophil recruitment and inflammation.

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41
Q

Name a member of the IL-17 family and its function.

A

IL-17A promotes the expression of proinflammatory cytokines and recruitment of neutrophils.

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42
Q

What is the primary function of chemokines?

A

Promoting the movement of immune cells into and out of lymphoid organs.

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43
Q

Name a chemokine and its target cell.

A

CCL19 attracts dendritic cells to lymph nodes.

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44
Q

Which chemokine attracts neutrophils to the site of infection?

A

CXCL8 (IL-8)

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45
Q

What is the structural feature used to classify chemokines?

A

The arrangement of cysteine (C) residues forming disulfide bonds.

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46
Q

What cytokine induces the expression of proinflammatory cytokines in neutrophils?

A

IL-17A

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47
Q

How does IFN-γ affect macrophages?

A

It activates them for enhanced immune response.

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48
Q

What is the role of erythropoietin (EPO) in the cytokine family?

A

EPO stimulates red blood cell production.

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49
Q

Which cytokine family is involved in cell death and immune signaling?

A

TNF family

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50
Q

What receptor does IL-1 bind to initiate its signaling pathway?

A

IL-1R1

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51
Q

What is the effect of TNF-α on apoptosis?

A

It promotes cell death (apoptosis) as part of immune regulation.

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52
Q

Which cytokine is crucial for the immune system’s early response to viral infections?

A

IFN-α

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53
Q

How do Type III interferons (IFN-λ) function?

A

They are secreted by dendritic cells and play a role in antiviral defense.

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54
Q

What is the function of GM-CSF in the Class I cytokine family?

A

It stimulates the production and differentiation of white blood cells.

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55
Q

What is the role of IL-6 in the Class I cytokine family?

A

It is involved in immune response regulation and inflammation.

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56
Q

Which cells are primarily targeted by IL-17 family cytokines?

A

Neutrophils and other immune cells involved in inflammation.

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57
Q

How do chemokines like CCL19 and CXCL8 guide immune cells?

A

By attracting them to specific locations, such as infection sites or lymph nodes.

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58
Q

What is the first step in cytokine signaling?

A

Cytokine binding induces receptor dimerization.

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59
Q

What role do JAK kinases play in cytokine signaling?

A

JAK kinases phosphorylate each other and the receptor upon activation.

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60
Q

What happens after JAK kinases are activated?

A

They phosphorylate tyrosine residues on the receptor.

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61
Q

What is the role of STAT proteins in cytokine signaling?

A

STAT proteins bind to phosphorylated sites on the receptor.

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62
Q

How are STAT proteins activated?

A

STAT proteins are phosphorylated by JAK kinases.

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63
Q

What occurs after STAT proteins are phosphorylated?

A

Phosphorylated STAT proteins dimerize.

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64
Q

What is the final step in the JAK-STAT signaling pathway?

A

STAT dimers translocate to the nucleus to promote gene transcription.

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65
Q

What antimicrobial protein in the skin specifically targets E. coli?

A

Psoriasin

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66
Q

What is the function of RegIII protein in the intestine?

A

It prevents contact with epithelial cells and generates pores in the membrane.

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67
Q

What is the role of collectins (SP-A and SP-D) in the respiratory tract?

A

They block and modify surface components of encapsulated and non-encapsulated pathogens.

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68
Q

How do magainins in the skin attack pathogens?

A

They form pores by binding to acidic phospholipids in pathogen membranes.

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69
Q

What is the function of histatins in antimicrobial defense?

A

They interfere with mitochondrial ATP in fungi.

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70
Q

What is the function of defensins in the intestine?

A

They form pores by binding to acidic phospholipids in pathogen membranes.

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71
Q

What do Pattern Recognition Receptors (PRRs) recognize in pathogens?

A

Pathogen-associated molecular patterns (PAMPs).

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72
Q

Where are PRRs located in cells?

A

In the membrane (for extracellular pathogens), endosomes (for endocytosed pathogens), and the cytosol (for intracellular pathogens like bacteria and viruses).

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73
Q

What types of cells express PRRs?

A

Myeloid and lymphoid leukocytes, as well as epithelial cells exposed to infectious agents.

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74
Q

What structural feature characterizes Toll-like receptors (TLRs)?

A

Leucine-rich repeats (LRRs) that form a horseshoe shape.

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75
Q

How do Toll-like receptors (TLRs) dimerize upon ligand binding?

A

They form homodimers or heterodimers.

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76
Q

What types of pathogens do TLR2/1 and TLR4 recognize?

A

TLR2/1 recognizes gram-positive bacteria, while TLR4 recognizes gram-negative bacteria.

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77
Q

What signaling pathway is activated by membrane-bound Toll-like receptors (TLRs)?

A

Activation of AP-1 and NFκB.

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78
Q

What additional signaling pathway is activated by endosomal TLRs?

A

Activation of IRF (Interferon Regulatory Factor) in addition to AP-1 and NFκB.

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79
Q

What do C-type lectin receptors (CLRs) recognize?

A

Carbohydrate components of fungi, mycobacteria, viruses, parasites, and some allergens.

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80
Q

What immune response is triggered by C-type lectin receptors (CLRs)?

A

Generation of proinflammatory cytokines and activation of phagocytes.

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81
Q

What type of receptors are NOD-like receptors (NLRs)?

A

Cytosolic receptors.

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82
Q

What is the function of NOD1 and inflammasomes in the NLR family?

A

They generate antimicrobial proteins and peptides and activate autophagy to eliminate intracellular bacteria.

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83
Q

What is the specific function of the NLRP inflammasome?

A

It generates IL-1β and triggers pyroptosis through the formation of pores in the membrane.

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84
Q

What type of pathogens do NLRP inflammasomes respond to?

A

Intracellular pathogens such as bacteria and viruses.

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85
Q

What are the main effector mechanisms of the innate immune system after pathogen identification?

A

Antimicrobial peptides, cytokines, enzymes (iNOS, COX2), phagocytosis, autophagy, and cell death (NETosis, pyroptosis).

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86
Q

What antimicrobial peptides are produced by epithelial cells?

A

Defensins and cathelicidins.

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87
Q

What is the role of antimicrobial peptides in the immune response?

A

They inhibit and kill pathogens.

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88
Q

What cytokine is produced by infected cells to inhibit viral replication?

A

Interferon α/β.

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89
Q

What cells are activated by interferons in response to viral infections?

A

NK cells and macrophages.

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90
Q

What is the function of IL-1 in inflammation?

A

It regulates macrophage and lymphocyte activity and induces fever.

91
Q

How does IL-6 influence the immune system?

A

It promotes neutrophil production in the bone marrow and enhances the acute phase response in the liver.

92
Q

What is the effect of TNF-α on vascular endothelial cells?

A

It increases vascular permeability, leading to fluid loss and localized inflammation.

93
Q

What process is activated by phagocytes to eliminate pathogens?

A

Phagocytosis.

94
Q

How do lysosomes contribute to pathogen elimination during phagocytosis?

A

Lysosomes contain enzymes, antimicrobial proteins, and reactive oxygen and nitrogen species (ROS and RNS) to destroy pathogens.

95
Q

What triggers inflammation during an innate immune response?

A

Tissue damage and the release of proinflammatory mediators like cytokines, which increase blood flow and recruit immune cells to the site of infection.

96
Q

What are the four cardinal signs of acute inflammation?

A

Redness (erythema), heat, swelling, and pain.

97
Q

What mutation is associated with Crohn’s disease in the innate immune system?

A

Mutation in NOD2.

98
Q

How does a NOD2 mutation contribute to Crohn’s disease?

A

It reduces defensin secretion and alters the regulation of intestinal microbiota.

99
Q

What is the consequence of altered intestinal microbiota in Crohn’s disease?

A

It leads to increased Th1 and Th17 responses, producing proinflammatory cytokines like TNF-α and IL-17.

100
Q

What role does regulatory T cell (Treg) deficiency play in Crohn’s disease?

A

It exacerbates the proinflammatory response, contributing to disease progression.

101
Q

What genetic mutations increase susceptibility to viral infections?

A

Mutations in signaling proteins that mediate the antiviral effects of IFN-α and IFN-β.

102
Q

What is septic shock and what causes it in the immune system?

A

Septic shock is a life-threatening condition caused by an excessive immune response to infection, often triggered by LPS activating TLR4 and releasing TNF-α and IL-1β.

103
Q

What are the consequences of septic shock on the body?

A

It causes vasodilation, low blood pressure, vascular damage, and can result in circulatory and respiratory failure.

104
Q

How do regulatory mechanisms in the immune system prevent septic shock?

A

Endotoxin tolerance develops when macrophages are repeatedly exposed to LPS, leading to cytokine release followed by immune response inhibitors like IκB.

105
Q

What is the role of IL-10 in immune regulation?

A

IL-10 is an anti-inflammatory cytokine that helps modulate immune responses and prevent excessive inflammation.

106
Q

What is the function of pattern recognition receptors (PRRs) in immune regulation?

A

PRRs can work synergistically across different signaling pathways to enhance immune defense.

107
Q

How do some pathogens evade detection by pattern recognition receptors (PRRs)?

A

By mutations such as those in proteobacteria flagellin, which prevent recognition by TLR5.

108
Q

How do Helicobacter, Coxiella, and Legionella evade the immune system?

A

They alter their LPS so that it is not recognized by TLR4.

109
Q

What is an example of a viral evasion mechanism targeting TLRs?

A

Viruses like Ebola and influenza produce proteins that block RIG-I signaling, preventing the activation of antiviral responses.

110
Q

How does the Listeria bacterium evade immune destruction?

A

It escapes the phagosome into the cytosol to avoid lysosomal degradation.

111
Q

What role do dendritic cells play in bridging the innate and adaptive immune systems?

A

Dendritic cells secrete cytokines that influence the differentiation of T cells based on the type of pathogen detected.

112
Q

What cytokines are secreted by dendritic cells to promote Th1 differentiation?

A

IL-12 and IFN-γ.

113
Q

What is the function of IL-10 and TGF-β produced by dendritic cells?

A

They promote the differentiation of regulatory T cells (Tregs), which help suppress excessive immune responses.

114
Q

How do pathogens like Mycobacterium tuberculosis inhibit phagosome maturation?

A

They block fusion between phagosomes and lysosomes, preventing the acidification necessary for pathogen destruction.

115
Q

What are the three pathways of complement activation?

A

The classical pathway, lectin pathway, and alternative pathway.

116
Q

What is the key event where all complement activation pathways converge?

A

The cleavage of C3 into C3a and C3b.

117
Q

What triggers the classical pathway of complement activation?

A

The binding of antigen-antibody complexes to C1q.

118
Q

How is the lectin pathway activated?

A

By the binding of mannose-binding lectin (MBL) to microbial carbohydrates.

119
Q

What activates the alternative pathway of complement?

A

Spontaneous hydrolysis of C3 on microbial surfaces.

120
Q

What is the function of C3b in complement activation?

A

C3b opsonizes pathogens, marking them for phagocytosis, and contributes to the formation of the C5 convertase.

121
Q

Which complement component initiates the formation of the membrane attack complex (MAC)?

A

C5b.

122
Q

What role does C3a play in the immune response?

A

It acts as an anaphylatoxin, promoting inflammation by recruiting immune cells.

123
Q

What is the convertase of C3 in the alternative pathway?

A

C3bBb + properdin.

124
Q

What is the C3 convertase in the lectin and classical pathways?

A

C4b2b.

125
Q

Which convertase is responsible for the cleavage of C5 in the alternative pathway?

A

C3bBb3b.

126
Q

Which complement components form the membrane attack complex (MAC)?

A

C5b678 + polyC9.

127
Q

In complement activation, what role does the C5 convertase play?

A

It cleaves C5 into C5a and C5b, initiating the formation of the MAC.

128
Q

What initiates the lectin pathway of complement activation?

A

The binding of mannose-binding lectin (MBL) to microbial surfaces.

129
Q

How does the classical pathway of complement activation begin?

A

With the binding of antibodies (Ig) to antigens, followed by C1 binding.

130
Q

What is the lytic function of the immune system?

A

It refers to the destruction of cells or pathogens.

131
Q

What does the antimicrobial function of the immune system do?

A

It fights against and eliminates microorganisms.

132
Q

What role does the immune system play in proinflammatory responses?

A

It triggers inflammation as a response to infection or injury.

133
Q

What is the chemotactic function in the immune system?

A

It involves guiding immune cells to the site of infection or damage.

134
Q

How does the immune system function as an opsonizer?

A

It marks pathogens for destruction by phagocytes.

135
Q

How does the immune system modulate acquired immunity?

A

It adjusts and enhances the adaptive immune response based on prior exposure to antigens.

136
Q

What is the role of the immune system in the elimination of immune complexes?

A

It removes antigen-antibody complexes to prevent damage to tissues.

137
Q

What is the homeostatic function of the immune system?

A

It maintains balance and stability in the body’s internal environment.

138
Q

What protein blocks contact between epithelial cells and pathogens in the intestine?

A

RegIII

139
Q

What proteins block and modify surface components of pathogens in the respiratory tract?

A

Collectins (SP-A and SP-D)

140
Q

What is the function of magainins in the skin?

A

They bind to acidic phospholipids in pathogens and form pores.

141
Q

What effect do histatins have on fungi?

A

They interfere with mitochondrial ATP in fungi.

142
Q

How do PRRs differ based on their location?

A

PRRs are found in the membrane (for extracellular pathogens), endosomes/lysosomes (for endocytosed pathogens), and the cytosol (for intracellular bacteria or viruses).

143
Q

What do Toll-like receptors (TLRs) recognize?

A

Leucine-rich repeats (LRRs).

144
Q

What PRRs induce the activation of AP-1 and NFκB?

A

Membrane-bound PRRs.

145
Q

What is the function of NOD receptors?

A

They generate antimicrobial proteins and peptides and activate autophagy to eliminate intracellular bacteria.

146
Q

What does the NOD2 gene mutation cause in Crohn’s disease?

A

A reduction in defensin secretion and alteration of the intestinal microbiota.

147
Q

What is the main defect in innate immune susceptibility to viral diseases?

A

Mutation in proteins that interfere with the antiviral effects of IFN-α and IFN-β.

148
Q

What activates TLRs during septic shock?

A

LPS activates TLR4, releasing TNF-α and IL-1β.

149
Q

How do pathogens evade immune destruction?

A

Through mechanisms like avoiding detection by PRRs, blocking signaling pathways, and preventing inhibition of replication.

150
Q

What is the common convergence point in complement pathways?

A

The C3 convertase.

151
Q

What are the three pathways of complement activation?

A

Classical pathway, lectin pathway, and alternative pathway.

152
Q

What are the main functions of complement?

A

Lytic, antimicrobial, proinflammatory, chemotactic, opsonizing, modulation of acquired immunity, elimination of immune complexes, and homeostatic.

153
Q

What triggers the activation of the classical complement pathway?

A

Antigen-antibody complexes binding to C1q.

154
Q

What role do C3a and C5a play in complement activation?

A

They induce inflammation and chemotaxis.

155
Q

What induces immune complex elimination in the complement system?

A

C3b binding to CR1.

156
Q

What pathogens alter complement signaling?

A

Viruses, bacteria, and fungi can block activation pathways or inhibit complement proteins.

157
Q

Where are B lymphocytes generated?

A

In the bone marrow.

158
Q

What is the primary function of B lymphocytes?

A

To produce antibodies.

159
Q

What happens to B lymphocytes that are not activated in time?

A

They undergo apoptosis.

160
Q

Why is B cell activation important?

A

It produces effector cells that secrete antibodies and memory cells for future infections.

161
Q

What are antibodies and what is their function?

A

Antibodies are proteins that bind to antigens to facilitate their destruction.

162
Q

What type of B cell activation is independent of the thymus?

A

Thymus-independent activation.

163
Q

What type of antibodies are produced by B-1 lymphocytes during thymus-independent activation?

A

IgM and sometimes IgA.

164
Q

What is the main difference between thymus-independent and thymus-dependent B cell activation?

A

Thymus-dependent activation involves T helper cells and produces a more specific and lasting response.

165
Q

What processes occur in thymus-dependent activation of B-2 lymphocytes?

A

Somatic hypermutation and class switching of antibodies.

166
Q

What antibodies are produced after thymus-dependent activation?

A

IgG or IgA.

167
Q

What is the difference between plasma cells and memory B cells?

A

Plasma cells secrete antibodies, while memory B cells remain for future immune responses.

168
Q

What is the basis of the effectiveness of vaccines?

A

The rapid response of memory B cells upon re-exposure to the same antigen.

169
Q

What B lymphocytes are involved in innate humoral immunity?

A

B-1 lymphocytes.

170
Q

How do B-2 lymphocytes interact with T helper cells?

A

Through complex immune synapses to activate a specific immune response.

171
Q

What function does immune memory serve in the body?

A

It allows a faster and stronger response upon re-encounter with the same antigen.

172
Q

What is the difference in antibody production between thymus-independent and thymus-dependent activation?

A

Thymus-independent activation produces antibodies with lower affinity, while thymus-dependent produces more refined and effective antibodies.

173
Q

What is the antimicrobial protein in the skin that specifically targets E. coli?

A

Psoriasin

174
Q

What protein prevents contact between epithelial cells and pathogens in the intestine?

A

RegIII

175
Q

What proteins block and modify surface components of pathogens in the respiratory tract?

A

Collectins (SP-A and SP-D)

176
Q

What function does magainin have in the skin?

A

It binds to acidic phospholipids of pathogens and forms pores.

177
Q

What effect do histatins have on fungi?

A

They interfere with mitochondrial ATP production.

178
Q

How do PRRs differ based on their location?

A

PRRs are located in the membrane (extracellular pathogens), endosomes/lysosomes (endocytosed pathogens), and cytosol (intracellular bacteria or viruses).

179
Q

What do Toll-like receptors (TLRs) recognize?

A

Leucine-rich repeats (LRRs).

180
Q

What PRRs induce the activation of AP-1 and NFκB?

A

Plasma membrane receptors.

181
Q

What function do NOD-like receptors (NODs) have?

A

They generate antimicrobial proteins and peptides and activate autophagy to eliminate intracellular bacteria.

182
Q

What causes the mutation in the NOD2 gene in Crohn’s disease?

A

Reduction in defensin secretion and alteration of intestinal microbiota.

183
Q

What is the primary defect in susceptibility to viral diseases related to the innate immune system?

A

Mutation in signaling proteins that mediate the antiviral effects of IFN-α and IFN-β.

184
Q

What triggers TLR activation during septic shock?

A

LPS activates TLR4, releasing TNF-α and IL-1β.

185
Q

How do pathogens avoid destruction by the immune system?

A

Through mechanisms like avoiding PRR detection, blocking signaling pathways, and preventing replication inhibition.

186
Q

What is the common convergence point of complement activation pathways?

A

The C3 convertase.

187
Q

What are the three pathways of complement activation?

A

Classical pathway, lectin pathway, and alternative pathway.

188
Q

What are the main functions of complement?

A

Lytic, antimicrobial, proinflammatory, chemotactic, opsonizing, modulation of acquired immunity, immune complex elimination, and homeostatic functions.

189
Q

What activates the classical complement pathway?

A

Antigen-antibody complexes binding to C1q.

190
Q

What role do C3a and C5a play in complement activation?

A

They induce inflammation and chemotaxis.

191
Q

What induces immune complex elimination in the complement system?

A

C3b binding to CR1.

192
Q

What pathogens alter complement signaling?

A

Viruses, bacteria, and fungi can block signaling pathways or inhibit complement proteins.

193
Q

Where are B lymphocytes generated?

A

In the bone marrow.

194
Q

What is the primary function of B lymphocytes?

A

To produce antibodies.

195
Q

What happens to B lymphocytes that do not activate in time?

A

They undergo apoptosis.

196
Q

Why is B cell activation important?

A

It produces effector cells that secrete antibodies and memory cells for future immune responses.

197
Q

What are antibodies and what is their function?

A

Antibodies are proteins that bind to antigens to facilitate their destruction.

198
Q

What type of B cell activation is independent of the thymus?

A

Thymus-independent activation.

199
Q

What antibodies are produced by B-1 lymphocytes in thymus-independent activation?

A

IgM and sometimes IgA.

200
Q

What is the main difference between thymus-independent and thymus-dependent B cell activation?

A

Thymus-dependent activation involves T helper cells and produces a more specific and lasting immune response.

201
Q

What processes occur in thymus-dependent B cell activation?

A

Somatic hypermutation and class switching.

202
Q

What antibodies are produced after thymus-dependent activation?

A

IgG or IgA.

203
Q

What is the difference between plasma cells and memory B cells?

A

Plasma cells secrete antibodies, while memory B cells persist for future immune responses.

204
Q

What is the basis for the effectiveness of vaccines?

A

The rapid response of memory B cells when re-exposed to the same antigen.

205
Q

What B lymphocytes are involved in innate humoral immunity?

A

B-1 lymphocytes.

206
Q

How do B-2 lymphocytes interact with T helper cells?

A

Through complex immune synapses to activate a specific immune response.

207
Q

What function does immune memory serve in the body?

A

It allows a faster and stronger response upon re-encounter with the same antigen.

208
Q

What is the difference in antibody production between thymus-independent and thymus-dependent activation?

A

Thymus-independent activation produces antibodies with lower affinity, while thymus-dependent activation produces more refined and effective antibodies.

209
Q

What is V(D)J recombination?

A

A process that combines V, D, and J segments to generate antibody and T-cell receptor diversity.

210
Q

What are the three types of genetic segments involved in V(D)J recombination?

A

V (Variable), D (Diversity), and J (Joining) segments.

211
Q

What function does V(D)J recombination serve in the immune system?

A

It generates antibody and T-cell receptor diversity to recognize multiple antigens.

212
Q

What are the four main processes of V(D)J recombination?

A

Synapsis, cleavage, processing, and joining.

213
Q

What happens during synapsis in V(D)J recombination?

A

The V, D, and J segments are selected and brought together.

214
Q

What is the role of RAG1 and RAG2 proteins in V(D)J recombination?

A

They initiate recombination by recognizing recombination signal sequences (RSS).

215
Q

What role does the enzyme TdT play in V(D)J recombination?

A

It adds random nucleotides to DNA breaks, introducing diversity.

216
Q

What do DNA repair proteins like ligase IV and Artemis do in V(D)J recombination?

A

They repair and join DNA ends after cleavage.

217
Q

What are recombination signal sequences (RSS)?

A

Sequences that indicate where DNA should be cut and joined during V(D)J recombination.

218
Q

What function do endonucleases and exonucleases have in V(D)J recombination?

A

They cleave and modify DNA ends to allow effective recombination.

219
Q

Where is the most variability generated during V(D)J recombination?

A

In the CDR3 region, where random nucleotides are added.

220
Q

What proteins are responsible for ligating DNA ends after V(D)J recombination?

A

DNA ligase IV and XRCC4.

221
Q

What do TdT and other enzymes introduce during recombination to increase diversity?

A

Random nucleotides.

222
Q

What happens if DNA repair fails during V(D)J recombination?

A

It can lead to defects in antibody and T-cell receptor formation.

223
Q

What is the final result of V(D)J recombination in terms of diversity?

A

A wide variety of antibodies and T-cell receptors that improve immune system responsiveness.

inmuno (6 decks)

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