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Immuno > Immunology Wk. 12 > Flashcards

Immunology Wk. 12 Flashcards

1
Q

Cancer Immunoediting & Equilibrium

● Immunoediting:
what are the 3 phases called and what (basically) happens?

A

● Immunoediting:
1. Elimination Phase- tumor cells killed by NK, CD4+, and CD8+
2. Equilibrium Phase- when the immune system is unable to
destroy the tumor
3. Escape Phase- appearance of clinically detectable tumors

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2
Q

Cancer Immunoediting & Equilibrium
● Equilibrium

what is another word for this and what is it?

A

● Equilibrium (aka Cancer Persistence)
○ State in which tumor cells remain but DO NOT progress
○ Steady State

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3
Q

Tumor Immunotherapy

is this unique or associated with other therapies?
what are the 2 types of immunization?

A

Tumor Immunotherapy
● Usually associated with other therapies
● Passive Immunization
● Active Immunization

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4
Q

Tumor Immunotherapy
● Passive Immunization
Specific or General?
examples?
● Active Immunization
are cells modified? if so how?
how does the vaccination wor?
what are some examples?

A

Tumor Immunotherapy
● Usually associated with other therapies
● Passive Immunization:
○ Non-specific immune stimulation
○ Examples:
■ Cytokine therapy
■ T-cell therapy
■ Monoclonal Ab against tumoral Ag
● Active Immunization:
○ Chemically modified tumor cells
○ Vaccination against oncogenic viruses (Ex: FeLV, Marek’s disease)

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5
Q

Immunomodulation

definition?

A

● Def: Use of agents to improve or suppress the immune
response

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6
Q

Immunomodulation
what are the 2 kinds and how are they distinguished?

A

● Def: Use of agents to improve or suppress the immune
response
● #1- Immunosuppression
○ Non-specific
○ Selective
● #2- Immunopotentiation -> stimulation of IR
○ Bacterial Products
○ Complex Carbohydrates
○ Vitamins A, D, & E
○ Cytokines: IL-2 and recombinant IFN

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7
Q

Non-Specific Immunosuppression
what are the 3 types?

A

● Radiation
● Corticosteroids
● Cytotoxic drugs

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8
Q

Non-Specific Immunosuppression
Radiation
how does it work/what does it do (generally)

A

● Radiation: prevents cell division

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9
Q

Non-Specific Immunosuppression
Corticosteroids
what do they do and how do they work?

A

Corticosteroids: produce I- kappa beta alpha (inhibitor of NF-
kappa Beta)

○ Blocks cytokine synthesis AND T cell response!

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10
Q

Non-Specific Immunosuppression
Cytotoxic drugs
what are the 3 and how do they work?

A

Cytotoxic drugs
○ Alkylating Agents= cross link DNA to prevent cell division
○ Folic Acid Antagonists= block tetrahydrofolate production (needed nucleotide
production)
○ DNA Synthesis inhibitors= inhibit DNA and RNA synthesis

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11
Q

Selective Immunosuppression
Name 3 and what they do

A

● Calcineurin Inhibitors:
○ Cyclosporine and Tacrolimus 🡪 BLOCK IL-2 PRODUCTION
● Rapamycin: blocks mTOR
○ mTOR= regulator for cell metabolism/growth
● JAK Inhibitors:
○ Inhibit mainly JAK1
○ Tx for atopic dermatitis (oclacitinib aka Apoquel)

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12
Q

Immunity Against Bacteria and Fungi
Bacteria
universal or specific response?
Gram pos/neg?
intra/extra cellular?
endo/exo toxin?
Aerobic/anaerobic?

what does recognition of bacteria called/lead to?

what 3 things are involved with PPR?

A

Bacteria

● The immune system will have different mechanisms to mount a
response against each type of bacteria
● Gram pos. vs Gram neg.
● Intracellular vs extracellular
● Exotoxin vs endotoxin
● Aerobic vs anaerobic
● Recognition of bacteria—>PRRs
○ (Pattern recognition receptors)
● Types or PRR, location, type of microbes

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13
Q

Immunity Against BacT
Innate IS
what recognizes what?
what releases?
how does !L-23 result in neutrophils?
Some bacterian increases what?
NK–> ?
compliment activation through what 2 pathways?

A

Innate Innate IS

● TLR recognize PAMPs
● Inflammation and cytokine release
● IL-23—>TH-17—>IL-17—>neutrophils
● Some bacteria increase NKG2D ligands
○ NK—>IFN-y—>macrophages and DC
● Complement activation
○ Alternative and Lectin pathwaysIS

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14
Q

Immunity Against BacT
Adaptive IS
● 5 basic effector mechanics:
what are they?

A

Adaptive IS
● 5 basic effector mechanics:
1. Neutralize toxins/enzymes
2. Classical complement pathway (IgG
and IgM)
3. Opsonization—>phagocytosis
4. Destruction of intracellular
bacteria—> T cell activated
macrophages
5. Direct killing by CD8 and NK cells

see diagram p.12

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15
Q

Bacteria

● #1- Toxigenic bacteria
what must happen to toxins?
AB neutralize and then what?

A

● #1- Toxigenic bacteria
○ Toxins need to be neutralized so they can’t do damage
○ AB neutralize and then phagocytosed by macrophages

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16
Q

Bacteria
● #2- Extracellular bacteria—> ?
wha tdo the antibodies do?
what sort of activation?

A

● #2- Extracellular bacteria—>HUMORAL
○ Opsonization by antibodies
○ Complement activation

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17
Q

Bacteria
● #3- Intracellular bacteria—> ?
what role do macrophages play and what is the process to get to CD8
what about ADCC aid, NK cells and Neutrophils?

A

● #3- Intracellular bacteria—>CELLULAR
○ Destruction of bacteria by macrophages (M1)
○ Macrophage is a APC—> MHC 1—>CD8
○ Direct killing by CD8
○ ADCC aid NK cell and neutrophils

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18
Q

Evasion by Bacteria
Extracellular

what 2 things are avoided in extracellular evasion of bacteria?

A

Avoiding phagocytosis
Avoiding complement

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19
Q

Evasion by Bacteria
Extracellular
Avoiding phagocytosis
4 things that occur:

A

Evasion by Bacteria
Extracellular
● Avoiding phagocytosis
○ Invades non-phagocytic cells
○ Surface inhibitors of phagocytosis
○ Secrete Exotoxin that kill phagocytic
cells
○ Capsule: poor phagocyte adherence

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20
Q

Evasion by Bacteria
Extracellular
● Avoiding complement
what three things occur?

A

● Avoiding complement
○ Bacterial products accelerate
breakdown of complement
○ Deviate the complement effectors
away from bacterial cell wall
○ Capsule prevent stable binding and
prevent formation of MAC

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21
Q

Evasion by Bacteria
Intracellular
what happens at the phagosome
what is prevented
what is resisted re: enzymes? what kind of enzymes?
what is inhibited?

A

Intracellular
● Escape phagosome and enter
cytoplasm
● Prevent formation of
phagolysosomes
● Resistance to lysosomal enzymes
● Inhibit M1

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22
Q

Fungi
what 3 kinds of infection?

A

● 1. Skin and other surface infection
● 2. Respiratory infection
● 3. Secondary infections by opportunistic fungi in
immunosuppressed animals

23
Q

Fungi

● 1. Skin and other surface infection
what occurs with the Nk cell
what occurs with the Th17

A

● 1. Skin and other surface infection
○ NK cell—>fungal destruction
○ Th17—>neutrophil rich acute inflammation—>fungal destruction

24
Q

Fungi
● 2. Respiratory infection

what occurs with Th1
Th17

A

● 2. Respiratory infection
○ Th1—>form granuloma—>fungal destruction
○ Th17—>neutrophil rich acute inflammation response—>fungal destruction

25
Q

Fungi
● 3. Secondary infections by opportunistic fungi in
immunosuppressed animals
what is relevent about Th1

A

● 3. Secondary infections by opportunistic fungi in
immunosuppressed animals
○ Th1 most effective due to secretion of IFN-y

26
Q

Viruses
Non-living—> ?
what don’t they have?
what 3 things should you know regarding obligate intracellular?
wht is virion?

A

● Non-living—> genome, protein coat,
other layers
● No organelles ● OBLIGATE intracellular ○ Can’t synthesize proteins on their
own
○ Outside host cell=dormant or
inert
○ Don’t multiply via division,
assembly line in host cell
● VIRION—>complete virus particle
(infective form)

27
Q

Immunity to Viruses
Intra & Extracellular
● Extracellular
what happens to Ab
phagocytosis?
what is damaged, how?

A

Immunity to Viruses

Intra & Extracellular
● Extracellular:
○ Neutralize Ab
○ Phagocytosis
○ Damage From Complement

28
Q

Immunity to Viruses

Intra & Extracellular
● Intracellular
what cells/structures are relevant?

A

○ NK cells
○ CD8+ cells
○ Macrophages

29
Q

Immunity to Viruses
Innate IS
what 2 systems with PRR regognize viral DNA/RNA?

A

Innate IS
● Recognize viral DNA/RNA—2
systems with PRR
● 1. RIG-1 and MDA5
● 2. TLRs
○ TLR3=dsRNA
○ TLR7 and 8= ssRNA
○ TLR9=unmethylated CpG (virus
and bacteria)

30
Q

Interferons
Type 1 interferons (IFN-a and IFN-B)
produced by what? when?
when do they peak?
what pathway resusts in what synthesis?

A

Interferons
● Type 1 interferons (IFN-a and IFN-B)
○ Produced by virus-infected cells within hours of invasion
○ Peak levels in the first days
○ JAK/STAT signaling pathway—> inhibit protein synthesis

31
Q

Interferons
● IFN-a—> ?

A

● IFN-a—> plasmacytoid DC
○ Lymphocyte, monocytes, and macrophage

32
Q

Interferons
● IFN-B—> ?

A

● IFN-B—> virus infected fibroblast

33
Q

Interferons
what cells do they activate?

A

● Activate NK cells

34
Q

Interferons
how do they transition re: immunity?

A

● Transition from innate to adaptive immunity

35
Q

Adaptive Immunity
Humoral Immunity
2 classifications?

A

● Antibodies against capsid
and envelope proteins
● Antibodies against proteins
expressed uninfected cells

36
Q

Adaptive Immunity
Humoral Immunity
● Antibodies against capsid
and envelope proteins
what happens to cell evasion?
what happens to phagocytosis?
what happens to the compliment?
what happens with viral clumping?

A

Adaptive Immunity
Humoral Immunity
● Antibodies against capsid
and envelope proteins
○ Prevent cell invasion by block
absorption
○ Stimulate phagocytosis
○ Trigger complement-mediated
viral lysis
○ Causing viral clumping

37
Q

Adaptive Immunity
Humoral Immunity
● Antibodies against proteins
expressed uninfected cells
what 2 things occur here?

A

● Antibodies against proteins
expressed uninfected cells
○ Complement-mediated
○ ADCC

38
Q

Adaptive Immunity
Cellular Immunity
How important is this for controlling viral disease?
how does MH1 work?
what happens to activated macrophages?
what is the relationship between virus and superagents?

A

Cellular Immunity
● MOST IMPORTANT FOR
CONTROLLING VIRAL
DISEASE
● MHC 1—>CD8
○ T cell derived IFN-y and TNF-a
● Activated
macrophages—>IFN-y
● Some virus can act as
superantigens 🡪
○ Th2 non-specific response

39
Q

Viral Evasion of Immune Response
Are they uniform for all virus?
RNA –> ?
what is antigenic variation?
example?

● DNA virus—>
what do they regulate?
what response to antigen processing pathways?
What do they prevent?
what relevance NK?
where do they go?

A

Viral Evasion of Immune Response
● Different virus have different strategies
● RNA virus—>small genome
○ Antigenic variation as the main mechanism
■ EX: influenza virus
● genetic drift-> pt mutations
● genetic shift-> reassortment of gene segments

● DNA virus—> larger genome
○ Negative cytokines regulation
○ Interfere with antigen processing pathway
○ Prevent apoptosis
○ NK evasion
○ Latency (hide in cells)

40
Q

Parasites
● HELMINTHS
2 catagories?

A

○ Innate
○ Adaptive

41
Q

Parasites

● HELMINTHS
Innate
explain what is produced, how?

A

Parasites

● HELMINTHS
○ Innate
■ Chitinases produced by mast
cells, macrophages, and
neutrophils
■ Cuticle—>chitin

42
Q

Parasites

● HELMINTHS
○ Adaptive
what response?
what are the 2 targets and what is the process for each?

A

○ Adaptive
■ Th2 response
■ 2 targets
■ Larvae—>eosinophils—>destru
ction
■ Adult worms—> IgE and
cytokines 🡪 expulsion

43
Q

Parasites
● ARTHROPODS
examples?
where are they found?
what is the process?
what result?

A

● ARTHROPODS
○ Ticks, mosquitos, flies, fleas
○ Saliva
○ Th2—>igE—> type 1
hypersensitivity
○ Mange (demodex)—> CD8 cells
(type IV)

44
Q

Parasites
● PROTOZOA
what are the 2 types?
describe?
how do they vary?

A

● PROTOZOA
○ Innate
■ Similar to bacteria
○ Adaptive
■ Th1 vs Th2

● Varies based on parasit

45
Q

Parasitic Escape of the Immune System
what are the 6 ways?

A

Parasitic Escape of the Immune System

● Resistance to effector mechanisms
● Avoid antigen recognition
● Block antigen recognition and processing
● Interfere with cell maturation
● Interfere with cell signaling
● Enhance regulation

46
Q

Which of the following blocks mTOR?

A. Calcineurin Inhibitors

B. Rapamycin
C. JAK-STAT Inhibitors
D. None of the above

A

B. Rapamycin

47
Q

WHICH OF THE FOLLOWING CELLS WILL
NOT AID IN THE REMOVAL OF TUMOR CELLS?

A. Antibodies
B. Th2
C. Th1
D. NK cells

A

B. Th2
Recall: Th2 cells can activate M2 macrophages—> M2 macrophages
can help tumors grow by stimulating VEGF and TGF-B

48
Q

WHICH OF THE FOLLOWING SELECTIVE
IMMUNOSUPPRESSION AGENTS IS
USEFUL FOR ATOPIC DERMATITIS?

A. Calcurin

B. DNA synthesis inhibitors

C. Rapamycin
D. JAK STAT inhibitor

A

D. JAK STAT inhibitor

49
Q

WHICH OF THE FOLLOWING IS MOST
HELPFUL AGAINST BACTERIA?

A. Th2
B. Th1
C. CD8+
D. Th17

A

D. Th17
TH17—>IL17—>Neutrophils—>BACTERIA

50
Q

WHICH OF THE FOLLOWING IS AN
INNATE RESPONSE TO BACTERIA?

A. Neutralization of toxins

B. Classical components of activation

C. TLR recognizing PAMPs

D. Destruction of intracellular bacteria via macrophages

A

C. TLR recognizing PAMPs

51
Q

WHICH OF THE FOLLOWING DOESN’T
PLAY A ROLE IN FUNGAL REMOVAL?

A. Th1
B. Th2
C. Th17

D. All of the above play a role

A

B. Th2

52
Q

WHAT IS NOT TRUE ABOUT A VIRUS?

A. Intracellular Pathogens
B. Non-living entity

C. They can synthesize proteins to replicate
D. The virion is the infective form of a virus

A

C. They can synthesize proteins to replicate
No they do not! They use host proteins to assembly line multiply

53
Q

WHAT IS THE MOST IMPORTANT
CELLULAR RESPONSE TO VIRUS?

A. Ab against capsid and envelope

B. CD8+

C. Ab against proteins

D. NK cells

A

B. CD8+
Cellular=T cells

CD8 via MHC 1 can destroy intracellular pathogens

54
Q

WHICH OF THE FOLLOWING

SENSITIVITY REACTIONS PLAYS A ROLE
IN MOSQUITO BITES AND FLEAS?

A. Type 1
B. Type 2
C. Type 3
D. Type 4

A

A. Type 1
Type 1—> atopy/allergies to the saliva
Mange (demodex)—> type 4—>delayed

Immuno (13 decks)

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