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Immunology > Immunology Exam I > Flashcards

Immunology Exam I Flashcards

1
Q

Where is the immune system?

A

Blood Stream

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2
Q

Primary Lymphoid Organs

A

Thymus - T cells
Bone Marrow - B cells

Site where white blood cells develop

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3
Q

Secondary Lymphoid Organs

A

Spleen
Lymph nodes
Tonsils

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4
Q

Hemopoietic stem cell –> common lymphoid progenitor –>

A

B cell / Plasma cell

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5
Q

Hemopoietic stem cell –> common lymphoid progenitor –> NK/T cell precursor –>

A

T cell/Effector cell

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6
Q

Common Myeloid Progenitor

A

I. Granulocyte
- neutrophil
- basophil
- eosinophil

II. Unknown Precursor
- monocyte –> dendritic cell + macrophage
- mast cell

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7
Q

cytokines

A

Molecules secreted by one cell and acting on another.

“Hormones of the immune system”

Can cause inactivation and Activation

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8
Q

Lymphocytes

A

T cells, B cells, NK cells

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9
Q

Proportion of Neutrophils

A

40-75%

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10
Q

Proportion of eosinophils

A

1-6%

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11
Q

Proportion of Basophils

A

<1%

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12
Q

Proportion of monocytes

A

2-10%

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13
Q

Proportion of Lymphocytes

A

20-50%

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14
Q

Cells of the Innate Immune System

A

Phagocytes
Granulocytes
NK Cells

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15
Q

Phagocytes

A

Macrophages
Neutrophils
Dendritic Cells

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16
Q

Granulocytes

A

Neutrophils
Basophils
Eosinophils
Mast Cells

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17
Q

Cells of the Adaptive Immunity

A

B and T cells

Proliferate + expansion of cells bound to the virus

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18
Q

Adaptive Immunity

A

Cells w/ exquisitely specific receptors for a potentially unlimited # of targets

T and B cells

Effective only after a delay of several hours/days

Recognizes only specific species

Immunity Increases because more memory cells remember the pathogen

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19
Q

Innate Immunity

A

Molecules and cells that distinguish host from infectious agents by recognizing conserved motifs
- fx: all gram negative bacteria

Activated within min to hrs of exposure

Not significantly increased after several exposures

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20
Q

Forms of Adaptive Immunity

A

Humoral Immunity - B cells - Antibody Response

Cell Mediated Immunity - T cells + cytokimes

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21
Q

B cells

A

Secreted or on cell surface
Two antigen binding sites

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22
Q

T cells receptor

A

Always on cell surface
One Antigen binding site

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23
Q

Antigen

A

A molecule (often derived from a pathogen) recognized by the immune system

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24
Q

Antibody

A

protein produced by B-cells, binds very specifically to a given antigen; also called immunoglobin

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25
Q

Epitope

A

Specific region of antigen. The region of an antigen that is bound to an antibody

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26
Q

Neutrophils are stored in

A

bone marrow and secreted to epithelial region upon infection

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27
Q

Macrophage Uptake

A

Uptake of bacteria causes change in gene expression of that macrophage leading to production of inflammatory cytokines

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28
Q

Transition from Innate –> Adaptive

A

Begins with the immigration of dendritic cells to the draining lymph nodes.

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29
Q

Myeloid lineage

A

Mast cell
Basophil
Eosinophil
Neutrophil
Macrophage
Dendritic Cell

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30
Q

Cells capable of phagocytosis

A

Dendritic Cells
Macrophage
Neutrophil

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31
Q

Eosinophils

A

Bi-lobed

Granules stain brightly with the dye, Eosin (ACID LOVING)

Granules contain a variety of toxic enzymes and histamine

Best known for combatting multicellular parasites or helminths (parasitic worms)

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32
Q

Basophils

A

Stain dark purple; with basic dye

Least common granulocyte

Granules contain histamine, proteoglycans (heparin and chondroitin) and proteolytic enzymes

Important source of the cytokine IL-4 which is central to allergic reactions (Starting the reaction)

Express IgE receptors like mast cells

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33
Q

Mast Cells

A

Major mediator of type I hypersensitivity rxns (Allergy)

Localized in tissues where they mature

Very similar to basophils

Granules contain histamine and heparin

Express receptors of IgE

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34
Q

Macrophages and Dendritic Cells

A

Phagocytic

Macrophages have bactericidal activity and can be present antigens under certain conditions

Dendritic cells are phagocytic, but not known for bactericidal activity

Dendritic cells are “professional antigen presenting cells” - they can stimulate T cells

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35
Q

Neutrophils

A

Poly-morpho nuclear cells (PNM)

Abundant in the blood

24h half life ( constantly regenerated)

Migrate from blood to sites of infection rapidly

Potent killers of pathogens
- phagocytosis
- granules loaded with degradative enzymes
- produce reactive oxygen and nitrogen radicals and other bactericidal compounds

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36
Q

Three Major Neutrophil Functions

A

Migration
Phagocytosis
Respiratory Burst (NADPH oxidase)

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37
Q

Migration

A

Leukocyte extravasation –> Movement of leukocytes out of the circulatory system and toward sites of inflammation or infections

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38
Q

Selectins

A

Enable initial attachment of leukocytes from the bloodstream

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39
Q

Low Affinity Integrin - Adhesion Molecule

A

LFA-1

Can do both high and low affinity conformation

Chemokine sends out information to the neutrophil to change the conformation of LFA-1 to high affinity conformation –> slows down.

Results in ICAM-1 –> Leukocytes stops

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40
Q

Phagocytosis and degranulation

A

Microbes bind to phagocyte receptors on neutrophil

Phagocyte membrane zips up around the microbe

Microbe ingested in phagosome

Fusion of phagosome with lysosome

Killing of microbes by ROS, NO and lysosomal enzymes in phagolysosomes

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41
Q

Phagocyte oxidase/ NADPH

A

yields Reactive Oxygen Species (ROS)

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42
Q

iNOS yields

A

Nitrogen radicals (NO)

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43
Q

What are in granules?

A

Enzymes –> degrade bacterial components

Defensins –> poke holes in bacterial membranes

Lactoferrin –> sequester iron away from bacteria

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44
Q

NADPH oxidase components

A

Secondary (specific) granules

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45
Q

Respiratory Burst

A

mediated by NADPH oxidase

Production of bactericidal compounds begins

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46
Q

Components of the NADPH oxidase complex

A

Localized to the membrane and in the cytoplasm (inactivated complex)

When cell becomes activated, these two components become co-localized and this is when the production of the radicals occur.

Gives rise to hydrogen peroxide and hypochlorous acid

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47
Q

bacterial killing cell types

A

macrophages and neutrophils

differ: neutrophils are short lived and produce oxygen radicals

Macrophage: produce mostly nitric oxide (nitrogen radical)

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48
Q

Neutrophil Death

A

apoptosis lyses the cell nucleus and plasma membrane. these small parts can be eaten by macrophage ingestion to clear out the dead neutrophil

If there has been an infectious event, neutrophils exist the body as pus

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49
Q

Chronic Granulomatous Disease (CGD)

A

NADPH oxidase defects

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50
Q

Chediak-Higashi syndrome

A

Phagocytosis and granule defects

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51
Q

Leukocyte Adhesion Deficiency (LAD)

A

deficiency in adhesion molecules, migration into tissues is minimal

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52
Q

zymogens (complement system)

A

an enzyme that is synthesized in serum, in a biologically inactive form, and must be cleaved in order to become biologically active

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53
Q

Function of complement system

A
  1. Control of inflammation (recruitment of phagocytes)
  2. Enhanced uptake and clearance (Opsonization)
  3. Lytic attack of cell membranes (killing bacteria)
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54
Q

Classical Pathway Activation

A

Antigen:antibody complex

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55
Q

MBL Pathway Activation

A

Lectin binding to pathogen surfaces

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56
Q

Alternative Pathway Activation

A

Pathogen Surfaces

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57
Q

What pathway happens spontaneously on pathogen surfaces?

A

The Alternative Pathway

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58
Q

All three pathways come together, resulting in

A

Complement activation

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59
Q

The Classical Pathway

A

Initiated by antibody or C reactive Protein (CRP) binding to pathogen surface

Initiation complex includes C1 components (C1q, C1r, C1s)

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60
Q

C1r + C1s

A

enzymatic components. must be cleaved to facilitate the cascade continuing

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61
Q

C1q

A

stalk like legs. attaches to the antigen binding site.
C1q is recruited to the bacterial surface.

Followed by activation of C1r and C1s

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62
Q

example of anaphylatoxin

A

c3a

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63
Q

What is an anaphylatoxin

A

molecule that recruits phagocytes to the site

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64
Q

c3b serves as an

A

opsonin

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65
Q

The MBL (mannose binding lectin) pathway is initiated by

A

MBL binding to specific mannose and fucose residues on pathogen surface ( consistent pattern)

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66
Q

What does the MBL initiating complex consist of?

A

MASP (MASP1, MASP2), proteins, and MBL

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67
Q

Step 1 of MBL (after initation)

A

Activated MASP2 cleaves C4 into C4a and C4b. Some C4b binds covalently to the microbial surface

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68
Q

Step 2 of MBL (after initiation)

A

Activated MASP 2 also cleaves C2 into C2a and C2b

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69
Q

Step 3 of MBL (after initiation)

A

C2a binds to surface C4b forming the classical C3 convertase C4b2a

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70
Q

Step 4 of MBL (after initiation)

A

C4b2a binds C3 and cleaves it to C3a and C3b. C3b binds covalently to the microbial surface

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71
Q

The Alternative Pathway Characteristics

A

I. Activation cascade is initiated without a ligand binding molecule

II. Complement is fixed on bacterial surfaces spontaneously

III. C3 Convertase is distinct from classical and MBL pathways

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72
Q

Spontaneous Activation og C3 in Plasma

A

The alternative pathway:

C3 is spontaneously hydrolyzed in serum and the end result is C3b which can attach to the bacterial membrane and liberation of C3a which acts as a chemoattractant (anaphylatoxin) to phagocytes

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73
Q

Enzymes in the Alternative Pathway

A

B and D factor

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74
Q

C3a anaphylatoxin

A

Tells the phagocytes to move to the site of the infection

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75
Q

The alternative C3 activation is

A

self perpetuating

76
Q

Classical + MBL C3 Convertase Components

A

C2a + C4b

77
Q

Alternative C3 Convertase Components

A

Bb + C3b

78
Q

C3a and C5a

A

Anaphylatoxins that act on blood vessels to increase vascular permeability

Move cells in a chemotactic fashion

Responsible for moving plasma, monocytes and proteins out of the vessel to engulf the nearby bacteria

79
Q

CR1 receptor

A

Binds the bacteria (tagged with C3b) to the macrophage surface

The macrophage performs endocytosis

macrophage membrane fuse, creating a membrane bound vesicle, the phagosome

lysosomes fuse with the phagosomes forming the phagolysosome

80
Q

C3 cleavage leads to

A

C3a –> recruits phagocytes
C3b –> tags bacterium for destruction (oposonization or membrane attack)

81
Q

C5b

A

binds to the bacterial membrane and initiates the assembly of “the membrane attack complex “ also called MAC.

82
Q

C5b binds firstly to

A

C6 and C7. These allow the C5 protein to anchor into the bacterial surface

Then C8 is recruited

83
Q

When C8 has been recruited..

A

Many C9 molecules are recruited to come in and form a pore in the bacterial surface.

84
Q

Membrane Attack results in

A

Leakage of the contents of the bacteria and disruption of the chemo-osmotic barrier and the bacteria dies

85
Q

Lytic Membrane Attack components

A

C5b - initiating ligand
C6
C7
C8
C9 - pore forming

86
Q

Which inhibitor acts in the early complement cascade?

A

C1 inhibitor (C1INH)

binds to activated C1r, C1s, removing them from C1q, (Shuts off the classical pathway)

and to activated MASP-2, removing it from MBL (Shuts off MBL pathway)

87
Q

Which inhibitor acts in the middle of the complement cascade?

A

Factor H (H) and Factor (I)

When one is lacking, the other cannot work.

88
Q

Factor H

A

binds C3b, displacing Bb; cofactor for I
Stops cascade from proceeding to membrane attack

89
Q

Factor I

A

Serine protease that cleaves C3b and C4b; aided by H, MCP, C4BP, or CR1

90
Q

Which inhibitor works in the late complement cascade?

A

CD59 (Protectin)

Prevents formation of membrane attack complex on autologous or allogeneic cells. Widely expressed on membranes

Binds to C9 - preventing pore formation

91
Q

H and I inactivation of C3b

A

C3b unable to continue in its cascade towards membrane attack, when I comes in and cleaves it. It can no longer be a ligand leading to membrane attack

92
Q

Factor I and H, DAF, MCP

A

inhibit complement on host cell membrane

results in iC3b

93
Q

Properdin

A

helps complement work on bacterial membranes.

stabilizes C3 convertase C3bBb on pathogen surface

94
Q

How does CD59 work?

A

CD59 comes in and binds to C5b678 complex and prevents recruitment of C9 to form the pore

95
Q

The Acute Phase Response

A

IL6 cause the liver to produce more MBL and CRP and fibrinogen. Increases the complement cascade components

96
Q

Job of C3a

A

Recruitment of inflammatory cells

97
Q

C3b serves as an

A

opsonin

98
Q

Effects of Deficiency: Immune-complex disease

A

C1, C2, C4

99
Q

Effects of deficiency: Susceptibility to capsulated bacteria

A

C3

100
Q

Effects of Deficiency: Susceptibility to Neisseria

A

C5-C9

101
Q

Effects of Deficiency: Similar effects to deficiency of C3

A

Factor I

102
Q

PAMPs

A

Pathogen associated molecular patterns

103
Q

PAMP of (gram +)

A

peptidoglycan, lipotheichoic acid

104
Q

PAMP bacteria

A

Hypomethylated CpG DNA

105
Q

Gram (-) PAMP

A

Lipopolysaccharide

106
Q

PAMP of motile organisms

A

Flagella –> Flagellin

107
Q

PAMPS are recognized by

A

Pattern recognition receptors (PRR) on cells of the innate immune system:

Macrophages, NK cells, neutrophils, dendritic cells

108
Q

PRRs include:

A

TLR (Toll like receptors)
Cytosolic Receptors

109
Q

Uptake receptors

A

Facilitate uptake of particles: complement receptors, scavenger receptors, mannose receptors

110
Q

Signaling Receptors

A

Recognizes bacterial PAMPs and induce activation of the cell through signaling cascades leading to changes in gene expression

TLR, NOD-like receptors, RIG-I-like receptors

111
Q

scavenger receptors

A

bind to carbohydrate residues

112
Q

Signaling receptors induce…

A

activation of the cell of the innate immune system

113
Q

Receptors in the cytoplasm

A

NOD like receptors
RIG-I-Receptors

114
Q

Membrane bound receptor

A

Toll Like Receptors (TLR)

115
Q

TLR Family names after the Toll Gene in

A

Drosophilia

116
Q

Structure of TLR

A
  • Transmembrane molecules
  • C terminus in cytoplasm (TIR Domain)
  • N Terminus in extracellular space ( Pathogen recognition domain)
117
Q

TIR domain (c terminus)

A

signaling domain on cytoplasmic end of the molecule and is specialized in binding to signaling proteins and starting signaling cascades

118
Q

Receptor TLR2

A

Ligands: Lipoteichoic acid
Microorganism recognized: Gram (+) bacteria

119
Q

Receptor TLR4 homo-dimer

A

Ligand: Lipopolysaccharide
Microorganism recognized: Gram negative bacteria

120
Q

Receptors TLR7 and TLR8, homo-dimers

A

Ligands: single stranded viral RNAs
Microorganisms recognized: RNA virus

121
Q

Receptor TLR9

A

Ligand: Un-methylated (hypo methylated) CpG-rich DNA
Microorganisms recognized: Bacteria

122
Q

Receptor TLR3

A

Ligand: Double stranded viral RNA
Microorganism recognized: RNA virus

123
Q

TLR 5 receptor

A

Ligands: Flagellin, a protein
Microorganisms recognized: Bacteria

124
Q

TLR that live in endosomes

A

Their ligands are nucleic acids, they can only access these when a pathogen has been pretty well degraded beforehand

125
Q

what TLRs are in the endosomes

A

TLR3,7,8,9

126
Q

TLR4 and TLR5

A

Live on plasma membrane
TLR4 recognizes LPS
TLR5 recognizes Flagellin

127
Q

TLR2 recognzies

A

Lipoteichoic acid at the cell surface

128
Q

What TLR needs help from other molecules to get access to LPS?

A

TLR4

129
Q

Molecules that help TLR4 access LPS from pathogens

A

LBP,CD14,MD2

130
Q

Why does TLR4 need help from three molecules to access LPS

A

Because LPS is lipophilic

131
Q

LBP

A

Binds and extracts LPS from the bacterial membrane, and takes it to TLR4

132
Q

MD2 and CD14

A

make it possible for TLR4 to become activated and recognize LPS

133
Q

TIR domain of TLR4 binds to

A

MyD88

134
Q

The interaction between the TIR domain and the MyD88 recruits

A

several kinases which turns on a kinase cascade

135
Q

at the end of the kinase cascade initiated by TIR and MyD88

A

Transcription factor NFkB becomes activated

136
Q

When NFkB is actiavted

A

moves to nucleus and initiates the expressing of several genes. Those genes are involved in inflammation and take the form as secreted cytokines

137
Q

TLR4 signaling by the TRIF and MyD88 pathway leads to

A

synthesis and secretion of TNF-alpha and other inflammatory cytokines

138
Q

PRR of the cytoplasm

A

NLR (bacterial)
RIGI (viral)
MDA5 (viral)
Inflammasomes (synthesis of biologically active IL1)

139
Q

NOD Like receptors NLR recognize

A

bacterial cell wall

140
Q

inflammasomes recognize

A

pathogens + intracellular damage or injury

141
Q

RIGI and MDA5 recognize

A

Viral nucleic acids

142
Q

NLRP3 (inflammasome) living in the cytoplasm

A
  • oligomerizes
  • activating pro-caspace 1
  • becomes active caspace 1
  • active caspace 1 can activate IL1B and
  • IL1B becomes biologically active
    -IL1B binds to receptor
  • Initiates inflammation
143
Q

IL1/IL6/TNF-alpha

A

Acts on:

Liver
Bone marrow endothelium
Hypothalamus
Fat, Muscle

144
Q

IL1/IL6/TNF-alpha

Liver

A

Acute phase proteins (CRP + Mannose binding lectin)

145
Q

IL1/IL6/TNF-alpha

Liver –> activation of

A

Complement opsonization

146
Q

IL1/IL6/TNF-alpha

Bone Marrow Endothelium

A

Neutrophil mobilization

leading to phagocytosis

147
Q

IL1/IL6/TNF-alpha

Hypothalamus

A

Increased body temperature,

leading to decreased viral and bacterial replication

148
Q

IL1/IL6/TNF-alpha

Fat and Muscle

A

protein and energy mobilization to generate increased body temperature

149
Q

IL1/IL6/TNF-alpha

Fat and Muscle

A

protein and energy mobilization to generate increased body temperature

leading to decreased viral and bacterial replication

150
Q

Dendritic Cell Maturation

Immature state

A

Tissue resident, resting

Highly endocytic

Low level expression of molecules and cytokines

Poor stimulators of T cells

151
Q

What turns a dendritic cell from immature to mature?

A

exposure to inflammatory stimuli, PAMPs

152
Q

Dendritic Cell Maturation

Mature State

A

Homes to lymph node

Endocytosis shut down

High level expression of molecules and cytokines

Highly stimulated for T cells

153
Q

Anti Viral Innate Immune Response

A

Type I interferon (beta and alphas)

Produced in response to viral infection

Acts in autocrine and paracrine manner to protect from further viral infection

154
Q

Autocrine

A

Feeds back on cell that produced signal

155
Q

Paracrine

A

Cell that produced it, secreted it, and made it available to other cells in close proximity

156
Q

Viral Detection and Response activated

A

Transcription factor IRF - Interferon Response Factor

157
Q

IRF Transcription Factors

A

Interferon Response Factors

move to nucleus, once activated, and they active transcription of IFN-alpha and IFN-beta

158
Q

Virus enters cell, IRF3 turns on

A

IFN-Beta in the nucleus. Leads to secretion of a cytokine

159
Q

IRF7 synthesizes

A

IFN-alpha

160
Q

Paracrine effect can produce

A

an anti viral state

161
Q

upregulation of PKR

A

inhibition of viral protein synthesis

162
Q

2,5-oligo A Synthetase

A

degradation of Viral RNA

163
Q

Mx GTPases

A

inhibition of viral gene expression and virion assembly

164
Q

RIG-I Receptors facilitates two types of responses

A

Activated IRF3 –> produces type I interferon
activated NFkB –> induced expression of inflammatory cytokines

165
Q

TLR7 and 3 recognize

A

Viral RNA, nucleic acids

Induce strong type I interferon responses

166
Q

TLR3 is the only signaling adapter that doesn’t associate with

A

MyD88

It associates with TRIF

167
Q

NK Cells respond to

A

normal proteins on cell surfaces and abnormal proteins. NK cells have multiple receptors

168
Q

NK cells

A

Lymphocytes of the innate immune system

169
Q

NK cells activity

A

Killing activity is balanced by activating and inhibitory responses

170
Q

Macrophages vs NK cells

A

Macrophage: receptors recognize the cell surface carbohydrates of bacterial cells, not human cells

NK cells: receptors recognize changes at the surface of human cells that are caused by antiviral infections

171
Q

Type I interferon drives

A

proliferation of NK cells

172
Q

Function #1 of NK cells

A

killing infected or damaged cells

173
Q

NK cells type of receptors

A

Inhibitory and Activating receptors

174
Q

KIRs

A

Killer cell immunoglobin like receptor

175
Q

KIRs can be

A

activating or inhibitory, depending on their cytoplasmic tail

176
Q

Long tails on KIRs indicate

A

inhibitory receptor

177
Q

Short tails on KIRs indicate

A

short cytoplasmic tails, whig interact with adapter molecules to facilitate signaling

178
Q

Because activating receptors have a short cytoplasmic tail, they have to interact with

A

signaling adapting molecule, to exhibit a positive signal

179
Q

Inhibitory receptors bind to

A

normal MHC Class I

180
Q

NK cell mechanism of killing

A

Formation of NK killing “synapse”

Delivery of toxic molecules in their granules (
- perforin –> pore forming molecule), common with C9 of complement cascade
- granzymes - are delivered through the pore, active an apoptotic cascade, activate caspases
- DNA cleavage, nuclear fragmentation, membrane blebbing

  • apoptosis of target cell
181
Q

Perforin

A

pore forming molecule (oligomerizes)

182
Q

granzymes

A

initiate an apoptotic cascade

183
Q

Function #2 of NK cells

A

production of cytokines to activate macrophages

184
Q

NK cells produce

A

IFN-gamma (type II interferon)
To stimulate the killing activity of macrophages

185
Q

chemokines

A

recruitment and activation of leukocytes

186
Q

IL1, TNF-alpha, IL6

A

pro inflammatory cytokines

Immunology (18 decks)

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