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Immunology (Part Two) > 14a – Effector Immunity > Flashcards

14a – Effector Immunity Flashcards

1
Q

Phases of immune response:

A
  1. Antigen recognition
  2. Lymphocyte activation: clonal expansion and differentiation
  3. Antigen elimination
  4. Contraction (homeostasis): apoptosis
  5. Memory
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2
Q

Intracellular pathogen effector response:

A

-Th1-type
>cytotoxic T cells
>IFN-g
>NK cells

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3
Q

Extracellular pathogen effector response:

A

-Th2-type
>mainly Ab driven

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4
Q

Extracellular and mucosal effector response:

A

-Th17-type
>IL-17
>IL-23
>regulators of mucosal responses
>tolerance
>*if fails: often autoimmune disease

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5
Q

No danger signals effector response:

A

-T regulatory
>food antigens
>etc.

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6
Q

Viruses type of response:

A

-intracellular (Th1)

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7
Q

Bacteria type of response:

A

-extracellular (Th2)
-intracellular (Th1)

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8
Q

Parasites type of response:

A

-extracellular
-intracellular

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9
Q

Fungi type of response:

A

-extracellular

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10
Q

Viruses:

A

-require cell machinery for replication
-no metabolism
-proteins with some glycogen residues and a genome (ssRNA, dsRNA, ssDNA, dsDNA)
*obligate intracellular pathogens

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11
Q

Relationship between virus and host:

A

-symbiotic would be ideal, but not always the case
>retroviral integration into the genome (HIV or SIV)

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12
Q

Viruses shapes and sizes:

A

-highly organized but simple
-smallest: rhino (cold)
-biggest: smallpox
-some ‘naked’: capsid proteins with no envelop
-others ‘enveloped’

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13
Q

Virus, bacteria and macrophage sizes:

A

-viruses: 20-400nm
-E. coli: 1000-2000nm
-macrophage: 21000nm

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14
Q

‘life cycle’ of RNA viruses:

A

-when they leave the cell they can leave viral proteins on the cell surface that the NK cells recognize

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15
Q

Recognition of viral PAMPS: steps

A
  1. TLR or other PRR of viral genome in endosomes and cytoplasm
  2. Pro-inflammatory cytokines and type-1 interferons (IFN) are produced
  3. IFN-a and IFN-b establish an anti-viral state within the vicinity
  4. Immune cells recruited to site of infection
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16
Q

Pro-inflammatory cytokines and type 1 INFs:

A

-establish an environment that make it difficult for the virus to replicate
Ex. raise body temperature to make it more difficult for virus to replicate (Ex. fever)

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17
Q

Type 1 IFNS:

A

-IFN-a and IFN-b
-extremely important
*contain virus to prevent spread into blood (viremia) and other organs
*induce antiviral state

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18
Q

Anti-viral state: interferon response

A

-induce resistance to viral replication in all cells
-increase expression of ligands for receptors on NK cells
-activate NK cells to kill virus-infected cells

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19
Q

Respiratory viral infection in lung example:

A

-virus causes damage to lung
>lymphocytes are being induced in lymph node and migrate to site of infections=effectors

20
Q

CD4+ T effector in Th1 response

A

-secret IFN-gamma
>activates macrophages
>drive the Th1 response and enhance CD8+ T cell killing

21
Q

CD8+ T effector in Th1 response:

A

-recognize infected cells via MHCI peptide
-kill via perforin/granzyme and Fas-FasL

22
Q

B cells in Th1 response:

A

-IgG antibodies
>not as much compared to Th2 response
>need to neutralize virus that is leaving the cell
>opsonize viral antigen on the membrane of the infected cell

23
Q

Main mechanisms of Th1 immunity to overcome a viral infection:

A
  1. CD8 cytotoxicity
  2. Macrophage activation
  3. ADCC by NK cells
24
Q

ADCC:

A

-antibody dependant cell-mediated cytotoxicity
-NK have Fc receptors
>recognize specific Abs bound to infected cell=release of cytotoxic granules by NK to kill the infected cell

25
Q

Viral evolution leads to:

A

-immune evasion strategies
-ability to manipulate immunity

26
Q

Example of immune suppression:

A

-HIV
>integrates into genome of CD4+ T cells
>re-emerges and depletes T cell population leading to AIDS

27
Q

Example of cytokine storm:

A

-COVID-19 or 1918 pandemic influenza (Spanish flu)
>hyperactivation of inflammatory cytokine response (completely out of control!)

28
Q

Immune regulation by PRRSV:

A

-enveloped, positive stranded RNA virus
-range in disease severity (asymptomatic to 100% mortality in pigs)
-different strains

29
Q

What are the major contributors to PRRSV disease outcome?

A

-age
-strain
-presence of co-infection

30
Q

PRRSV syndromes:

A

-respiratory difficulty
-blue ear syndrome
-reproductive failure in sows

31
Q

Low virulent strains: PRRSV

A

-asymptomatic infection
-immune suppression
-hardly any inflammatory cytokines

32
Q

Chinese high path strains: PRRSV

A

-cytokine storms result in high mortality rates

33
Q

Immune regulation by viruses can be:

A

-overwhelming

34
Q

Bacteria recognition:

A

-conserved motifs recognized by TLRs
>LPS
>peptidoglycan
>CpG DNA

35
Q

Bacteria types:

A

-gram negative and positive
-cocci, bacilli, spiral shape
*all shapes, sizes and arrangements

36
Q

Bacteria modes of transmission:

A

*infections at different sites
-contamination of food
-instruments
-fomites
-direct contact
-aerosols

37
Q

Bacteria virulence mechanisms:

A

*different immune responses to bacteria species
-endotoxins (inside) and exotoxins (secreted)
-spores and biofilms
-granulomas (TB latency and immune evasion)
-intracellular cell-cell replication (syncytia)

38
Q

Innate response to bacteria: steps

A
  1. TLR recognition of PAMPS
  2. Macrophages triggered to release cytokines, chemokines and AMPs
  3. Vasodilation and increased vascular permeability (neutrophil and macrophage migration)
  4. Combination of phagocyte recruitment, cytokines, and AMPs=swelling, pain, heat and redness
39
Q

Alternative (innate) activation of complement: steps

A
  1. Conserved motifs on bacteria activate complement (alternative pathway)
  2. C3b can opsonize bacteria
  3. C3a and C5a are anaphylatoxins
  4. MAC punches holes in bacterial cell walls
40
Q

Anaphylatoxins:

A

-C3a and C5a
-promote inflammation
-phagocyte recruitment

41
Q

Th2 immunity to extracellular bacteria: APCs

A

-present bacterial peptide to CD4+ T cells
>activate Th cells to help
>produce Th2 cytokine (IL-4, IL-5, IL-13)
>activate B cells to produce antibodies

42
Q

Th2 immunity to extracellular bacteria: B cells

A

-activated by CD4+ Th cells and differentiated into plasma cells that produce Abs
>Abs pumped into lymph and blood

43
Q

Abs once pumped into lymph and blood:

A

-neutralize toxins
-agglutination of microbes
-opsonization
-neutralize bacterial attachment to cells
-activate complement (classical activation): lysis

44
Q

Th1 immunity to intracellular bacteria:

A

Ex. Salmonella, Mycobacterium
>can replicate within the cell
>TLR detect them and drive a Th1 type response (like viruses)

45
Q

Cell mediated immunity and IFN-gamma: (intracellular bacteria)

A

-necessary to activate macrophages to clear bacterial infection and kill infected cells

Immunology (Part Two) (18 decks)

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