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MICRO > Ch2: Innate Immunity > Flashcards

Ch2: Innate Immunity Flashcards

1
Q

What are the components of innate immunity? 8

A
  1. Anatomical barriers
  2. Antimicrobial substances
  3. Normal flora that competes with pathogens
  4. Immune cells
  5. Sensor systems
  6. Phagocytosis
  7. Inflammation
  8. Fever
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2
Q

What is the specificity of innate immunity?

A

Structures shared by classes of microbes or damaged cells

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3
Q

What is specificity of adaptive immunity?

A

Structural detail of microbial molecules (antigens)

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4
Q

Receptors for innate immunity are encoded where?

A

Germline

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5
Q

Which has more diverse receptors, innate or adaptive?

A

Adaptive

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6
Q

What encodes adaptive immunity receptors?

A

Genes produced by somatic recombination of gene segments

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7
Q

How is the distribution of receptors described in innate immunity?

A

Nonclonal: Identical receptors on all cells of same lineage

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8
Q

How is the distribution of receptors described in adaptive immunity?

A

Clonal: Clones of lymphocytes with distinct specificities express different receptors

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9
Q

Can both adaptive and innate immunity discriminate against self?

A

Yes

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10
Q

How long does innate immune response last?

A

From 0-4 hours

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11
Q

When does the early induced response occur?

A

4-96 hours

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12
Q

When does the adaptive immune response occur?

A

After 96 hours

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13
Q

What is the skin’s mechanical, chemical and microbiological barrier to infection?

A

Mechanical: Perspiration and sloughing
Chemical: Sebum and Defensins
Microbiological: Normal flora

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14
Q

What is the GI tract’s mechanical, chemical, and microbiological barrier to infection?

A

Mechanical: Flow of fluid/food
Chemical: Acidity, enzymes, defensins
Microbiological: Normal flora

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15
Q

What is the respiratory tract’s mechanical, chemical and microbiological barrier to infection?

A

Mechanical: Flow of fluid, mucus, air
Chemical: Lysozyme in nasal secretions & Defensins
Microbiological: Normal flora

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16
Q

What is the urogenital tract’s mechanical, chemical and microbiological barrier to infection?

A

Mechanical: Flow of fluid
Chemical: Acidity in vaginal secretions, spermine and zinc in semen, defensins
Microbiological: Normal flora of urogenital tract

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17
Q

What are the eyes’ mechanical, chemical and microbiological barrier to infection?

A

Mechanical: Flow of tears
Chemical: Lysozyme in tears, Defensins
Microbiological: Normal flora

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18
Q

What is mucin?

A

Host cell derived glycoproteins that coat pathogens and inhibit adherence

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19
Q

Acids and bile salts have what effect in stomach?

A

Make is difficult for organisms to move past stomach

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20
Q

What do lysozymes degrade?

A

Peptidoglycans

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21
Q

Function of lactoferrin?

A

Sequester iron so bacteria don’t have access

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22
Q

What are alpha and Beta defensins?

A

Cationic peptides that damage negatively-charged membranes

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23
Q

Defensins are comprised of what?

A

35-40 amino acids containin 3 intra-chain disulfide bonds

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24
Q

Charge of defensins?

Why is this important?

A

Positively

Can interact with negative charged membranes

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25
Q

Are defensins hydrophobic or hydrophilic?

A

Both: amphipathic

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26
Q

Function of defensins?

A

Disrupt membrane integrity of bacteria, viruses, and fungi

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27
Q

Defensins are formed as what first?

A

Inactive precursors

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28
Q

What is the main source of defensins in the intestine?

A

Paneth cells

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29
Q

When a bacteria enters a surface wound, what happens? 3

A
  1. Resident effector cells secrete cytokines
  2. Vasodilation and increased vascular permeability
  3. Tissue is inflamed
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30
Q

3 types of cells created from lymphoid progenitor cell?

A

B Cell
T Cell
NK Cell

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31
Q

B Cells do what?

A

Produce antibodies

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32
Q

What do B cells transform into?

A

Plasma cell

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33
Q

What do plasma cells do?

A

Secrete antibodies

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34
Q

What do natural killer cells do?

A

Kill cells infected with certain viruses

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35
Q

What does a neutrophil do?

A

Phagocytose microorganisms

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36
Q

What does an eosinophil do?

A

Kills antibody-coated parasites through release of granules

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37
Q

What does a basophil do?

A

Control immune response to parasites

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38
Q

What does a dendritic cell do? 2

A
  1. Activates T Cells

2. Initiates adaptive immune response

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39
Q

What does a mast cell do?

A

Expulsion of parasites from body through release of granules containing histamine

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40
Q

What is a monocyte?

A

Circulating precursor cell to macrophage

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41
Q

What does a macrophage do? 2

A
  1. Phagocytose microorganisms

2. Activates T cells –> Initiates immune response

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42
Q

What does a megakaryocyte do? 2

A
  1. Platelet formation and 2. wound repair
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43
Q

What does an erythrocyte do?

A

Oxygen transport

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44
Q

4 types of white blood cells?

A
  1. Granulocytes
  2. Mononuclear phagocytes
  3. Dendritic cells
  4. Lymphocytes
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45
Q

4 types of granulocytes

A
  1. Neutrophils
  2. Basophils
  3. Eosinophils
  4. Mast cells
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46
Q

What is the most abundant cell in innate response?

A

Neutrophil

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47
Q

How long relatively is a neutrophils life?

A

Short

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48
Q

What 3 granulocytes are involved in allergic reaction?

A
  1. Basophils
  2. Eosinophils
  3. Mast Cells
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49
Q

What common cell is a member of the mononuclear phagocyte system?

A

Monocytes

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50
Q

What differentiate from monocytes?

A

Macrophages

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51
Q

What are four common macrophages differentiated from blood monocyte?

A
  1. Microglia (CNS)
  2. Kupffer cell (Liver)
  3. Alveolar macrophage (Lung)
  4. Osteoclasts (bone)
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52
Q

Dendritic cells are involved in which immune response?

A

Adaptive

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53
Q

Dendritic cells do what?

A

Finds material in tissue and brings it to adaptive immunity cells

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54
Q

Lymphocytes are involved in which immune response?

A

Adaptive

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55
Q

What is main difference of Natural killer cells and T & B cells?

A

NK Cells don’t have specificity

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56
Q

What is first thing to happen when first line barriers are breanched?

A

Tissue-resident macrophages and complement recognize the material

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57
Q

Recognition by macrophage and complement leads to what? 4

A
  1. Macrophage cytokine production
  2. Cell migration
  3. Inflammation
  4. Initiation/activation of adaptive response
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58
Q

Macrophage cytokine production causes what? 2

A
  1. Host cells to produce cytokines

2. Induce expression of cell surface molecules by epithelial cells

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59
Q

E and P selectin are examples of what?

What do they do?

A

Cell surface molecules

Bind sialyl-Lewis

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60
Q

ICAM’s are examples of what?

What do they do?

A

Cell surface molecules

Bind integrins

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61
Q

5 main ways a pathogen is recognized?

A
  1. Mannose-binding lectin
  2. Macrophage mannose receptor
  3. Scavenger receptor
  4. Toll-like receptor
  5. Nucleotide-binding oligomerization domain protein
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62
Q

Mannose-binding lectin is found where?
Part of what family?
What does it bind?

A

Free plasma

Collagenous lectin (collectin) protein family

Carbohydrates expressed by pathogens

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63
Q

Define a lectin

A

Any protein that is not an antibody nor from the immune system but binds to carbohydrate-receptors on cell surfaces

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64
Q

Macrophage mannose receptor is what type of molecule?
What is it dependent on?
What does it bind to?

A

Lectin

Calcium

Sugars on pathogens

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65
Q

Scavenger receptors recognize what? (2)

A
  1. Anionic polymers

2. Acetylated low-density lipoproteins

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66
Q

Toll-like receptors recognize what?

A

PAMP’s

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67
Q

Nucleotide-binding oligomerization domain (NOD) proteins are similar to what?

A

TLR’s

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68
Q

Main effects of triggering receptors on macrophages? 2

A
  1. Increase phagocytosis

2. Increase proinflammatory cytokine production

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69
Q

Define phagocytes

A

Cells that engulf and digest microbes and cellular debris

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70
Q

Which phagocytes are found even in healthy tissues? (2)

A
  1. Macrophages

2. Dendritic cells

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71
Q

Which phagocyte only appears when needed?

A

Neutrophils

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72
Q

What bacteriocidal agents does a phagocyte have? 6

A
  1. Acidification
  2. Toxic oxygen-derived products
  3. Toxic NO
  4. Antimicrobial peptides: Defensins & Cationic
  5. Enzymes: Lysozyme and Hydrolases
  6. Competitors: Lactoferrin & VB12-BP
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73
Q

What is respiratory burst?

A

Rapid, transient release of ROS

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74
Q

What are the steps for producing ROS? 3

A
  1. In endocytic vacuole, NADPH oxidase produces superoxide.
  2. Superoxide dismutase converts this to peroxide
    3A. Peroxidase and iron convert this to hypochlorite and hydroxyl radicals
    3B. Catalase converts this to H2O and O2 to increase pH for activation of defensins and lysozymes
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75
Q

Nitric oxide production also occurs which is produced by what?

What induces this?

A

NO Synthase

IFN-Gamma

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76
Q

What type of receptor is a Toll-like receptor?

A

Pathogen recognition receptor

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77
Q

What do Toll-like receptors recognize?

A

PAMP’s

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78
Q

Toll-like receptors are expressed intracellularly or extracellularly?

A

Both

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79
Q

What do intracellular TLR’s usually recognize?

A

Nucleic acids

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80
Q

What TLR’s recognize bacterial lipopeptides?

A

TLR-1:TLR-2

TLR-2:TLR-6

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81
Q

What TLR’s recognize bacterial peptidoglycan

A

TLR-2

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82
Q

What TLR’s recognize LPS?

A

TLR-4

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83
Q

What TLR’s recognize bacterial flagellin?

A

TLR-4

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84
Q

What TLR recognizes dsRNA?

A

TLR-3

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85
Q

What TLR’s recognize ssRNA?

A

TLR-7 and TLR-8

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86
Q

What TLR’s recognize CpG DNA?

A

TLR-9

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87
Q

What bacteria will be noticed by TLR4?

Why?

A

Gram-negative bacteria

Have LPS

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88
Q

What is required for LPS recognition by TLR4? (3)

A

LPS-binding protein (LBP)
MD2
CD14

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89
Q

Steps of TLR activation and the result? 5

A
  1. TLR is engaged by bacteria or virus
  2. TIR signaling domain recruits adaptor proteins
  3. Activation of transcription factors occurs (NF-KB and IRF’s)
    4A. NF-KB causes an increase in expression of cytokines, adhesion molecules, costimulators
    4B. IRF’s cause a production of type 1 interferon (IFN alph/Beta)
    5A. Increased expression causes acute inflammation and stimulation of adaptive immunity
    5B. Production of IFN causes an antiviral state
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90
Q

What do cytokines do?

A

Bind to surface receptors and regulate cell function

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91
Q

What is cytokine redundancy?

A

Multiple cytokines perform similar functions

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92
Q

What does it mean if a cytokine is pleiotropic?

A

Single cytokine can stimulate multiple functions

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93
Q

What is a chemokine?

A

Cytokine important in chemotaxis

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94
Q

What is a colony stimulating factor?

A

Cytokine important in multiplication and differentiation of leukocytes

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95
Q

What is an interferon?

A

Important cytokine that controls viral infections and inflammatory response

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96
Q

What is a interleukin?

A

Important cytokine that is produced by leukocytes for both innate and adaptive immunity

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97
Q

What is tumor necrosis factor?

A

Cytokine that kills tumor cells and initiates inflammation

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98
Q

What are five common pro-inflammatory cytokines?

A 
IL-6
TNF-Alpha
IL-1Beta
CXCL8
IL-12
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99
Q

IL-6 has what effects? 2

A
  1. Fever

2. Acute-phase production production by hepatocytese

100
Q

TNF-alpha has what effects? 4

A
  1. Activation of vascular endothelium and increases vascular permeability –> complement and cells leak into tissue
  2. Fever
  3. Mobilization of metabolites
  4. Shock
101
Q

IL-1Beta has what effects?

A
  1. Activates vascular endothelium –> Leaking
  2. Activate lymphocytes
  3. Local tissue destruction
  4. Increase access of effector cells
  5. Fever
  6. Production of IL-6
102
Q

Function of CXCL8?

A
  1. Chemotaxic factor that recruits neutrophils and basophils to site of infection
103
Q

Function of IL-12?

A

Activate NK cells

104
Q

Function of IL-1, IL-6, and TNF-alpha in liver?

Which will cause what?

A

Activates acute-phase proteins (CRP, MBL)

Activation of complement and opsonization

105
Q

Function of IL-1, IL-6, and TNF-alpha in bone marrow?

Which will cause what?

A

Neutrophil mobilization

Phagocytosis

106
Q

Function of IL-1, IL-6, and TNF-alpha in hypothalamus?

Which will cause what? 3

A

Increased body temperature

Decrease pathogenic replication
Increased antigen processing
Increased specific immune response

107
Q

Function of IL-1, IL-6, and TNF-alpha in fat and muscle?

Which will cause what? 3

A

Protein and energy mobilization –> Increase body temp

Decrease pathogenic replication
Increased antigen processing
Increased specific immune response

108
Q

Function of IL-1, IL-6, and TNF-alpha in dendritic cells?

Which will cause what?

A

TNF-alpha stimualtes migration to lymph nodes and maturation.

Initiation of adaptive immune response

109
Q

Acute-phase proteins are produced by what?

110
Q

4 members of acute-phase proteins?

A
  1. Serum amyloid protein
  2. C-reactive protein
  3. Fibrinogen
  4. Collectin family
111
Q

Members of collectin family include? (3)

A
  1. Mannose-binding lectin
  2. SP-A
  3. SP-D
112
Q

What does C-reactive protein bind to?

A

Phosphocholine component of LPS in bacterial and fungal cell walls

113
Q

3 roles of inflammation?

A
  1. Deliver additional effector molecules to site
  2. Provide physical barrier of coagulation to prevent pathogen spreading
  3. Promote repair of injured tissue
114
Q

Which is bad, local or systemic infection?

115
Q

Explain why local infection leads to survival! 5

A
  1. Macrophage activated to secrete TNF-alpha in the tissue
  2. Increased release of plasma proteins, phagocytes, lymphocytes into tissue and platelet adhesion to blood vessel wall
  3. Phagocytosis of bacteria with local vessel occlusion cause containment of infection.
  4. Antigens drain and taken to lymph node
  5. Survival and stimulation of adaptive immune response
116
Q

Explain why systemic infection leads to death? 4

A
  1. Macrophages activated in liver and spleen secrete TNF-alpha into bloodstream
  2. Systemic edema causes decreased blood volume which collapses vessels
  3. Disseminated intravascular coagulation leads to wasting and multiple organ failure septic shock
  4. death
117
Q

4 types of adhesion molecules?

A
  1. Vascular addressin
  2. Selectin
  3. Integrin
  4. Immunoglobulin
118
Q

What do selectins bind?

A

Carbohydrates

119
Q

What do selectins initiate?

A

Leukocyte-endothelial interaction

120
Q

P-selectin is found where? What is its ligand?

A

Activated endothelium and platelets

PSGL-1
Sialyl Lewis

121
Q

E-selectin is found where? What is its ligand?

A

Activated endothelium

Sialyl Lewis

122
Q

What do integrins bind to? (2)

Function?

A

Cell-adhesion molecules and ECM

Strong adhesion

123
Q

What kind of cells contain integrins?

A

Monocytes, T Cells, macrophages, neutrophils, dendritic cells

124
Q

LFA-1 have what ligand?

125
Q

Mac-1 (CR3) has what ligands? (3)

A

ICAM-1
iC3b
Fibrinogen

126
Q

CR4 integrin has what ligand?

127
Q

VLA-5 has what ligand?

A

Fibronectin

128
Q

Function of immunoglobulin superfamily?

A

Various roles in cell adhesion by being ligands for integrins

129
Q

ICAM-1 is found where?

Ligands? (2)

A

Activated endothelium

LFA-1, Mac1

130
Q

ICAM-2 is found where?

Ligand?

A

Resting endothelium
Dendritic cells
LFA-1

131
Q

VCAM-1 is found where?

Ligand?

A

Activated endothelium

VLA-4

132
Q

PECAM is found where?

Ligand?

A

Activated leukocytes

Endothelial cell-cell junctions

133
Q

How do cells home to the site of infection?

A

Follow chemotactic gradient formed by CXCL8:CXCL8 receptor interactions

134
Q

4 steps of leukocyte getting to the site of infection

A
  1. Rolling by weakly binding cell addressin to endothelium selectin.
  2. Integrin activation by chemokines interacting with chemokine receptor on cell
  3. Integrin binds to endothelial ICAM tightly
  4. Migration through endothelium
135
Q

What activates the high affinity state of integrin:ICAM interactions?

A

Chemokines

136
Q

First cells to arrive at site of infection?

A

Neutrophils

137
Q

Where are neutrophil reserves stored?

A

Bone marrow

138
Q

What do neutrophils do upon reaching infection site?

A

Engulf and kill bacteria

Then die in the tissue and are engulfed and degraded by macrophages

139
Q

Neutrophil receptors recognize what?

Specifically what?

A

Pathogens

PAMP’s

140
Q

What receptors allow neutrophils to recognize complement components?

A

CR3 and CR4

141
Q

Can multiple receptors work at the same time in neutrophils?

142
Q

Azurophilic granules are filled with what?

A

Proteins and peptides that disrupt and digest microbes

143
Q

Examples of enzymes that digest microbes?

A
  1. Lysozyme
  2. Defensins
  3. Myeloperoxidase
  4. Neutral proteases (cathepsin G, elastase, proteinases)
  5. Bactericidal/permeability increasing protein
144
Q

Function of bactericidal/permeability-increasing protein?

A

Binds LPS and kills Gram-negative bacteria

145
Q

Effect of triggering receptors on macrophages?

A
  1. Increase phagocytosis

2. Increase proinflammatory cytokine production

146
Q

Complement is produced where?

147
Q

Result of complement activation (3)

A

Opsonophagocytosis
Inflammation
Lysis

148
Q

How many ways exist for complement to be activated

149
Q

Complement protein naturally exist how?

150
Q

What enzyme form are many complement proteins?

A

Serine proteases (cut proteins where serines exist)

151
Q

First serine protease in classical pathway is what?

152
Q

What does C1R doing its action represent?

A

Activating step of classical pathway of complement

153
Q

The C1 complex (contains C1R) binds what? 3

Via what

A
  1. IgM
  2. IgG1
  3. IgG3

C1q

154
Q

What are the three best antibody isotypes for capacity to fix complement?

A

IgM
IgG3
IgG1

155
Q

What are the steps of the classical pathway of complement? 7

A
  1. C1q recognizes antibodies on bacterial surface
  2. C1r cleaves itself, two C1s copies, and itself again
  3. C1s cleaves C4 into C4a and C4b
  4. C4b binds to pathogen surface
  5. C4b binds C2
  6. C1s cleaves C2 into C2a and C2b
  7. C4bC2a forms the classical C3 convertase and cleaves C3 into C3a and C3b
156
Q

How many C3 molecules can the classical C3 convertase cleave?

157
Q

C3a acts how?

A

Powerful chemoattractant for immune cells

158
Q

C3b acts how?

A

Powerful opsonin (coats pathogen for receptor recognition)

159
Q

What is the classical C5 convertase?

160
Q

How are host cells protected by C3b deposition?

A

The thioester bond on C3b is rapidly hydrolyzed if it does not react with a pathogen so that it cannot bind to human cells.

161
Q

What are the steps of C3b leading to opsonophagocytosis? 5

A
  1. Complement activation leads to C3b binding to bacteria
  2. CR1 on macrophages binds C3b
  3. Endocytosis of bacterium
  4. Phagosome is formed
  5. Lysosome fuses with phagosome to form phagolysosome
162
Q

C3a and C5a are both known as what?

A

Anaphylatoxins

163
Q

What do anaphylatoxins do? (4)

A
  1. Increase vascular permeability
  2. Increase cell adhesion molecule expression
  3. Cause smooth muscle contraction
  4. Release of histamine from mast cells
164
Q

The actions of anaphylatoxins lead to what?

A

Influx of antibodies, complement proteins, and cells to establish strong chemotactic gradient

165
Q

What are the steps of the formation of membrane attack complex? 2

A
  1. C5 convertase (C4bC2aC3b) cleaves C5 into C5a and c5b

2. C5b binds C6 to initiate MAC formation and lyse bacteria

166
Q

Most important part of formation of Membrane Attack Complex?

A

C9 because it forms membrane pores

167
Q

In absence of IgM or IgG what can initiate the classical complement pathway?

A

C-reactive protein binding to C1

168
Q

What type of molecule is C-reactive protein?

A

Acute phase protein made in liver

169
Q

Advantage of CRP binding and activating classical complement pathway?

A

In absence of antibody, as it typical in early infection, allows for classical pathway to be activated

170
Q

What does the Lectin pathway of complement activation use to initiate? 2

A

Mannose-binding lectin

Ficolins

171
Q

What do Mannose-binding lectin and Ficolins bind directly to?

A

Microbial sugars without needing pathogen specific antibody

172
Q

Mannose-binding lectins and ficolins are structurally similar to what?

173
Q

What acts as C1r and C1s in lectin pathway?

A

Mannose-binding lectin-associated proteases (MASP-1 and MASP-2)

174
Q

Steps of lectin pathway of complement activation? 6

A
  1. MASP-2 cleaves C4 to C4a and C4b
  2. C4b binds to microbial surface
  3. MASP-2 cleaves C2 to C2a and C2b
  4. C2a binds to C4b forming classical C3 convertase
  5. C4b2a binds C3 and cleaves it into C3b and C3a.
  6. C3b binds to microbial surface
175
Q

Main difference between Lectin pathway and Classical pathway?

A

C1 is not involved in lectin

176
Q

The alternative pathway lacks what molecule?

A

C1 or a Mannose-binding lectin

177
Q

Chronological order of the 3 complement activations?

A
  1. Alternative pathway
  2. Lectin pathway
  3. Classical pathway
178
Q

How is a C3 convertase generated in alternative pathway?

A
  1. C3 made in the liver
  2. Tickover (C3 thioester bond hydrolyzed without cleaved forming iC3)
  3. iC3 binds Factor B
  4. Factor B-iC3 bind Factor D
  5. Factor D cleaves Factor B into Ba and Bb
  6. Soluble iC3bBb is formed and cleaves C3 into C3a and C3b
  7. C3b is deposited into pathogen
  8. C3b finds Factor B
  9. Factor D cleaves Factor B into Ba and Bb to form C3bBb
179
Q

What is the alternative C3 convertase?

180
Q

What is the alternative C5 convertase?

181
Q

What does Properdin/Factor P do?

A

Stabilize C3bBb and extends its life –> increase C3b opsonization

182
Q

What does Factor H do?

A

Binds C3b and changes its conformation which allows Factor I to cleave it into iC3b (inactive) which will be involved in adaptive immunity

183
Q

What does Decay Accelerating factor (DAF) do?

A

Removes Bb from C3bBb making the alternative C3 convertase inactive

184
Q

Membrane cofactor protein (MCP) does what?

A

Removes Bb from C3b and allows Factor I to cleave C3b into iC3b which is inactive

185
Q

Where are DAF and MCP expressed?

Why?

A

Surface of healthy host cells

Prevent alternative pathway from acting on self

186
Q

What does C1 inhibitor do?

A

Inhibits C1r and C1s serine protease activity

187
Q

What does Factor I do?

A

Cleaves C3b and C4b

188
Q

What does C4-binding protein (C4BP) do?

A

Causes dissociation of classical pathway C3 convertase by assisting in cleavage of C4b

189
Q

What does CD59 do?

A

Blocks C9 binding and prevents formation of MAC

190
Q

What does Type 1 complement receptor do? (CR1)

A

Causes dissociation of C3 convertase subunits (C3b AND C4b)

191
Q

All 3 complement activation pathways converge where?

A

C3 convertase

192
Q

The C3b that is bound to surface of a cell initiates what?

A

Opsonization
Inflammation
Cell lysis

193
Q

Initiators of classical pathway include? (3)

194
Q

Initiators of Lectin pathway include? 2

A
  1. Mannose-binding lectins

2. Ficolins

195
Q

Initiator of alternative pathway is what?

196
Q

Does alternative pathway need antibody?

197
Q

Does alternative pathway need microbial sugar recognition?

198
Q

Does alternative pathway need inhibitors to prevent attack on self?

199
Q

C3b functions as what? (3)

A
  1. Opsonin
  2. Part of C3 convertase
  3. Part of C5 convertase
200
Q

C3a stimulates what?

A

Inflammation

201
Q

Factor B is so important for what role?

A

Active enzyme of C3 and C5 convertases

202
Q

Outome of complement opsonization and phagocytosis?

A

Phagocytosis and killing of microbe

203
Q

Outcome of complement-mediated cytolysis?

A

MAC complex allows for osmotic lysis of microbe

204
Q

Outcome of complement stimulation of inflammatory reactions?

A

Destruction of microbes by recruited leukocytes

205
Q

Initial serine protease in each pathway?

A

Classical: C1s
Lectin: MASP-2
Alternative: Factor D

206
Q

C3 convertase in each pathway?

A

Classical: C4b2a
Lectin: C4b2a
Alternative: C3bBb

207
Q

What is chronic granulomatous disease caused by?

A

Lack of NADPH oxidase –> no respiratory/oxidative burst

208
Q

What happens to bacteria in chronic granulomatous disease?

A

Taken up by macrophages but can’t be destroyed

209
Q

What is leukocyte adhesion deficiency the result of?

A

Malfunctioning cell adhesion molecules

210
Q

Result of leukocyte adhesion deficiency?

A

Cells can’t enter sites of infection = No recruitment

211
Q

Interleukin Receptor-Associated kinase deficiency is result of what?

A

Lack of response to TLR and IL-1

212
Q

Result of interleukin receptor-associated kinase deficiency?

A

Can’t initiate inflammatory response

213
Q

Result of disorder with C1q, C1s, C4?

A

Autoimmune (SLE, glomerulonephritis)

214
Q

Result of disorder with C3, C6, Factor I?

A

Recurrent bacterial infection

215
Q

Result of disorder with C1r, C2, C5, C7

A

Recurrent bacterial infections AND autoimmunity

216
Q

Result of disorder with C1INH

A

Can’t turn off C1 binding –> Hereditary angioedema

217
Q

A virus infected cell releases what?

A

Interferons

218
Q

What are interferons?

A

Cytokines that interrupt viral replication

219
Q

3 parts of Interferon response?

A
  1. Induce resistance to viral replication in all cells
  2. Increase expression of ligands for receptors on NK cells
  3. Activate NK cells to kill virus-infected cells
220
Q

What are the Type I interferons?

A

IFN-alpha

IFN-beta

221
Q

What is the Type II interferon?

222
Q

What is first group of molecules to be produced in response to virus?

A

IFN-alpha, IFN-Beta, TNF-alpha, IL-12

223
Q

What is second group of molecules to be produced in response to virus?

224
Q

What is third group of molecules to be produced in response to virus?

225
Q

NK cells have what two types of receptors on surface?

A
  1. Activating

2. Inhibitory

226
Q

Host cells have what type of proteins that will bind to NK cells?

A

Proteins that bind to inhibitory receptors on NK Cells

227
Q

What is the one activating receptor that can overcome all inhibitory signals on an NK Cell?

228
Q

2 classes of inhibitory and activating receptors on NK cells?

A

Immunoglobulin-like receptors

Lectin-like receptors

229
Q

Inhibitory NK cells naturally bind what?

A

Host MHC and receive negative signal

230
Q

In virus infected cells, what happens to MHC?

Result

A

Down-regulation of MHC expression

NK Cell loses negative signal

231
Q

Virus-infected cells express what protein at their surface?
Which binds to what?
Result?

A

MIC protein
Binds to activating receptor NKG2D
Positive signal sent to NK cell

232
Q

What is in the granules that NK cell releases?

A
  1. Perforin
  2. Granulysin
  3. Granzymes
233
Q

Main source of TNF? 2

Targets (6)

A

Macrophages and T cells

Endothelial cells: Activate
Neutrophils: Activate
Hypothalamus: fever
Liver: Make acute phase proteins
Muscle, fat: Catabolism
Many cells: Apoptosis
234
Q

Source of IL-1? (2)

Targets? 4

A

Macrophages and endothelial cells

Endothelial cells: Activate
Hypothalamus: Fever
Liver: Acute-phase protein synthesis
T cells: Differentiation

235
Q

Source of chemokines? 6

Target?

A
  1. Macrophages
  2. Dendritic cells
  3. Endothelial cells
  4. cells
  5. Fibroblasts
  6. Platelets

Leukocytes: Increase integrin affinity, chemotaxis, activation

236
Q

IL-12 source? (2)

Target? (2)

A
  1. Dendritic cells
  2. Macrophages
  3. NK Cells: Activation
  4. T Cells: Differentiation and activation
237
Q

IFN-gamma source? (2)

Target (2)

A
  1. NK cells
  2. T cells
  3. Activate macrophages
  4. Stimulate antibody response
238
Q

IFN-alpha source (2)

Target? (2)

A
  1. Dendritic cells
  2. Macrophages
  3. All cells: Antiviral state
  4. NK cells: activate
239
Q

IFN-beta source?

Target? (2)

A
  1. Fibroblasts
  2. All cells: Antiviral state
  3. NK cells: activate
240
Q

IL-10 source? (3)

Target? (2)

A
  1. Macrophages
  2. Dendriticl cells
  3. T cells

Macrophages and dendritic cells: Inhibit IL-12

241
Q

IL-6 source? (3)

Target? 2

A
  1. Macrophages
  2. Endothelial cells
  3. Liver: Acute phase proteins
  4. B cells: Proliferation
  5. T cells
242
Q

IL-15 source?

Target: (2)

A

Macrophages

  1. NK cells: Proliferation
  2. T cells: Proliferation
243
Q

IL-18 source?

Target? (2)

A

Macrophages

  1. NK cells: IFN-gamma synthesis
  2. T cells: IFN-gamma synthesis
244
Q

TGF-Beta source?

Target? (2)

A

Many cells

  1. Inhibition of inflammatin
  2. T cells: Differentiation
245
Q

Goal of innate defenses? 2

A
  1. Recognize infection

2. Limit and stop spread

246
Q

Initiators of inflammation are?

How so

A

Tissue macrophages

Release cytokines

247
Q

Complement helps clear infections when?

A

Before and after antibodies are produced

MICRO (22 decks)

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