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Microimm 2500 > (I) Lecture 3: Innate Immunity Part II > Flashcards

(I) Lecture 3: Innate Immunity Part II Flashcards

1
Q

Innate Immune Cell Differentiation

A

all start hematopoietic stem cell and then differentiate into myeloid and lymphoid progenitors which differentiate into phagocytes and lymphocytes respectively

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2
Q

Myeloid Origin Immune Cells

A

Neutrophils
Monocytes/Macrophages
Dendritic Cells

destroy EXTRACELLULAR pathogens by PHAGOCYTOSIS

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3
Q

Lymphoid Immune Cells

A

Natural Killer Cells

destroy INTRACELLULAR viruses by APOPTOSIS

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4
Q

How are pathogens detected?

A

Compromise of barrier = pathogens inside tissue = release of chemical signals sensed by cells in blood that swarm to site infection

Pathogen detections is needed to recruit and activate immune cells

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5
Q

PRRs

A

Pattern Recognition Receptors

  • expressed at the surface and within many cell types
  • recognize conserved, invariant regions of pathogens (don’t change and recognize broad patterns)
  • can also recognize damage/infection signals
  • specificity is germ-line encoded (doesn’t change from, birth)
  • triggers IMMEDIATE response
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6
Q

PAMPs

A

Pathogen Associated Molecular Patterns

  • what PRRs recognize
  • usually from extracellular pathogens
  • include sugars, lipids, proteins, viral nucleic acids
  • only expressed by pathogens (not self molecules)
  • highly conserved (low mutation rate). critical for microbial survival and pathogenesis
  • detection of PAMPs is critical to initiation of immune responses
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7
Q

Examples of PAMPs

A

Some are critical for microbe’s structure (integrity)
- ex. peptidoglycan in cell wall of gram + bacteria

Some are critical for microbe’s pathogenicity (ability to infect)
- ex. bacterial flagellin

Some are viral PAMPs
- ex. viral nucleic acids

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8
Q

PRRs and PAMPs

A
  • each TLR has distinct range of specificities
  • surface TLRs recognize components on the OUTSIDE of the pathogens (ex. peptidoglycan, flagellin)
  • endosomal TLRs recognize components released during DEGRADATION (ex. bacterial + viral nucleic acids)
  • one type of PRR can bind many different PAMPs (redundancy increases the range of pathogens that can be detected)
  • we only have limited # of PRRs (< 100)
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9
Q

Families of PRRs

A

4 families:
- Toll-like receptors (TLR)
- C-type lectin receptors (CLR)
- Nucleotide oligomerization receptors (NLR)
- RIG-I like receptors (RLR)

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10
Q

Candida albicans

A

opportunistic pathogen yeast in the human gut microbiome

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11
Q

How do PRRs bind PAMPs?

A
  1. Recognition: PRRs bind to PAMPs
  2. Pseudopods engulf pathogen: actin forms pseudopods which eat the pathogen
  3. Phagosome formation
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12
Q

Phagocytosis

A

Cell eating

Killing happens in the phagolysosome b/c the phagosome is not toxic w/o the lysosome

  1. Bacterium binds to PRRs on pseudopodia (membrane evaginations)
  2. Bacterium is ingested into phagosome
  3. Phagosome fuses w/ lysosome
  4. Bacterium is killed and digested by low pH-activated lysosomal enzymes
  5. Digestion products are released from cell
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13
Q

The Phagolysosome

A

Phagosome is innocuous but phagosome-lysosome fusion makes it highly bacteriocidal
- phagocytes engulf microbes and they are broken down in phagolysosomes

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14
Q

Antimicrobial Properties of Phagolysosome

A
  • low pH
  • NADPH oxidase = Reactive Oxygen Species (toxic)
  • Myeloperoxidase (MPO) transforms H2O2 into bleach
  • Lactoferrin captures Fe2+ needed for bacterial growth
  • Defensins form pores
  • Lysozyme degrades peptidoglycan
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15
Q

Most abundant leukocyte

A

Neutrophils

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16
Q

Neutrophils

A
  • majority (50-70%) of blood circulating leukocytes (WBCs)
  • exit blood and rapidly enter infected tissues
  • swarm in large numbers to site of infection to respond to inflammatory molecules
  • main component of PUS
  • life span is only a few days
17
Q

Neutropenia

A

Abnormally low levels of neutrophils

  • highly susceptible to deadly infections
  • can restore neutrophil levels via blood transfusion (of neutrophil rich blood)
  • if untreated, innate immune response can’t control infection so pathogen can spread rapidly, even into blood = septic shoc/neutropenic sepsis
18
Q

Macrophages

A

Professional phagocytes

  • remove pathogens and damaged host cells
  • differentiate from monocytes (when there is infection signal)
  • also works in adaptive immunity
  • have SPECIALIZED functions based on location
  • long life span (months to years)
19
Q

Dendritic Cells

A
  • bridge btwn innate and adaptive immunity
  • role and function depend on MATURATION STATE
20
Q

Maturation of Dendritic cells

A

Immature DC:
- circulate in blood AND reside in tissue below/among epithelial cells
- role in innate immunity (PHAGOCYTE)

Mature DC:
- initiates adaptive immunity
- antigen presentation

21
Q

Phagocytes Process of Action

A
  1. Tissue damage and bacteria cause chemoattractants and vasoactive factors to trigger a local increase in blood flow and capillary permeability
  2. Permeable capillaries allow influx of fluid and cells
  3. Neutrophils and other phagocytes migrate to site of inflammation (chemotaxis)
  4. Phagocytes and antibacterial substances destroy bacteria
22
Q

Natural Killer Cells

A

Cytotoxic cell killers that circulate in the blood

Kill INTRACELLULAR VIRUSES (virus-infected and cancer cells)

  • have granules that contain cytotoxic enzymes (perforin and granzyme) that cause cell death in target cells
  • early component of the response of viral infection
  • after cytokine release, a wave of NKC follows
23
Q

Perforin

A

In NKC

forms a pore in the cell membrane
- allows granzyme to enter the virus-infected cell

24
Q

Granzyme

A

In NKC

degrades nucleic acids and triggers APOPTOSIS

  • also degrades viral nucleic acids to PREVENT VIRAL REPLICATION
25
Q

NKC deficiency

A

Ppl w/ NKC deficiency are susceptible to frequent herpesvirus infections

26
Q

Destroying extracellular microbes

A

via PHAGOCYTOSIS

  • macrophages
  • neutrophils
    -dendritic cells
27
Q

Destroying intracellular viruses

A

via APOPTOSIS

Natural Killer Cells target virus-infected cells

28
Q

Destroying intracellular bacteria

A

NO innate mechanism to deal with them

good at avoiding phagocytosis

control of these bugs may require T-cell help from adaptive immune system

29
Q

Survival to phagocytosis

A

Intracellular bacteria can survive phagocytosis to live/replicate inside a phagocytes

  • bacteria can live in phagosome: inhibit lysosome-phagosome fusion
  • bacteria live in phagolysosome: resistant to lysosomal acids/enzymes

control of these bugs may require T cell help from adaptive immune system

30
Q

L. monocytogenes

A

Listeria (can survive in cytoplasm and spread cell to cell)

  1. InIA: internalization
    - lets it directly affect the cell
  2. LLO: Listeriolysin, degrades the phagolysosome
    - can escape to cytoplasm where it can survive
  3. ActA: Actin assembly-inducing protein
    - uses cell’s actin filaments to propel themselves to the next cell
    - big problem for pregnant ladies
31
Q

True or False

Innate immunity involves receptors formed prior to pathogen exposure

A

True

because they are germline-encoded from birth

32
Q

True or False

NK cells effectively kill intracellular bacteria

A

False

NO good innate response against intracellular bacteria

Microimm 2500 (29 decks)

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