Immunology Wk. 12 Flashcards by catherine perea

Cancer Immunoediting & Equilibrium

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

● 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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Cancer Immunoediting & Equilibrium
● Equilibrium

what is another word for this and what is it?

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

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Tumor Immunotherapy

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

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

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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?

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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Immunomodulation

definition?

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

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

● 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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Non-Specific Immunosuppression
what are the 3 types?

● Radiation
● Corticosteroids
● Cytotoxic drugs

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

● Radiation: prevents cell division

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

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

○ Blocks cytokine synthesis AND T cell response!

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

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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Selective Immunosuppression
Name 3 and what they do

● 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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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?

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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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?

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

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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Bacteria

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

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

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

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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?

● #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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Evasion by Bacteria
Extracellular

what 2 things are avoided in extracellular evasion of bacteria?

Avoiding phagocytosis
Avoiding complement

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Evasion by Bacteria
Extracellular
Avoiding phagocytosis
4 things that occur:

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

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

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

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Fungi
what 3 kinds of infection?

Study These Flashcards

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

Fungi

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

Study These Flashcards

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

Fungi
● 2. Respiratory infection

what occurs with Th1
Th17

Study These Flashcards

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

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

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

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

● 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)

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

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

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

○ NK cells ○ CD8+ cells ○ Macrophages

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

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)

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

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

Interferons ● IFN-a—> ?

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

Interferons ● IFN-B—> ?

● IFN-B—> virus infected fibroblast

Interferons what cells do they activate?

● Activate NK cells

Interferons how do they transition re: immunity?

● Transition from innate to adaptive immunity

Adaptive Immunity Humoral Immunity 2 classifications?

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

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?

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

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

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

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?

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

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?

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)

Parasites ● HELMINTHS 2 catagories?

○ Innate ○ Adaptive

Parasites ● HELMINTHS Innate explain what is produced, how?

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

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

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

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

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

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

● PROTOZOA ○ Innate ■ Similar to bacteria ○ Adaptive ■ Th1 vs Th2 ● Varies based on parasit

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

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

Which of the following blocks mTOR? A. Calcineurin Inhibitors B. Rapamycin C. JAK-STAT Inhibitors D. None of the above

B. Rapamycin

WHICH OF THE FOLLOWING CELLS WILL NOT AID IN THE REMOVAL OF TUMOR CELLS? A. Antibodies B. Th2 C. Th1 D. NK cells

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

WHICH OF THE FOLLOWING SELECTIVE IMMUNOSUPPRESSION AGENTS IS USEFUL FOR ATOPIC DERMATITIS? A. Calcurin B. DNA synthesis inhibitors C. Rapamycin D. JAK STAT inhibitor

D. JAK STAT inhibitor

WHICH OF THE FOLLOWING IS MOST HELPFUL AGAINST BACTERIA? A. Th2 B. Th1 C. CD8+ D. Th17

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

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

C. TLR recognizing PAMPs

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

B. Th2

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

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

WHAT IS THE MOST IMPORTANT CELLULAR RESPONSE TO VIRUS? A. Ab against capsid and envelope B. CD8+ C. Ab against proteins D. NK cells

B. CD8+ Cellular=T cells CD8 via MHC 1 can destroy intracellular pathogens

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

Immunology Wk. 12 Flashcards

(54 cards)