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Immunology > Ch. 5 Innate Immunity > Flashcards

Ch. 5 Innate Immunity Flashcards

1
Q

How does skin inhibit microbial growth and entry?

A
  • antimicrobial peptides, fatty acids in sebum
  • epidermis is tightly backed w/ keratin (waterproof)
  • oily, salty surface is also coated w/ antimicrobial peptides to inhibit unwanted microbes
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2
Q

How does the stomach inhibit microbial growth?

A

low pH, digestive enzymes, antimicrobial peptides, fluid flow toward intestine

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3
Q

How does the small intestine inhibit microbial growth?

A

digestive enzymes, antimicrobial peptides, fluid flow to large intestine

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4
Q

How does the urogenital tract inhibit microbial growth?

A

flushing by urine, aggregation by urinary mucins; low pH, antimicrobial peptides, vaginal secretions

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5
Q

How do the lungs inhibit microbial growth?

A

cilia sweep mucus outward, coughing, sneezing expels mucus, macrophages in alveoli

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6
Q

Lysozyme function

A

cleaves glycosidic bonds of peptidoglycans in cell walls of bacteria, leading to lysis

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7
Q

Lactoferrin function

A

binds and sequesters iron, limiting growth of bacteria and fungi, disrupts microbial membranes, limits infectivity of some viruses

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8
Q

Psoriasin function

A

disrupts membranes, killing cells; binds and sequesters divalent cations limiting growth of bacteria and fungi

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9
Q

Sp-A function

A

blocks bacterial surface components, promotes phagocytosis

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10
Q

How do defensins kill microbes?

A

disrupt membranes of bacteria, fungi, protozoan parasites, and viruses; additional toxic effects intracellulary; kill cells and disable viruses

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11
Q

How do cathelicidins kill microbes?

A

disrupts membranes of bacteria; additional toxic effects intracellulary; kills cells

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12
Q

How do dermicidns kill microbes?

A

antibacterial and antifungal; produces channels in membranes that disrupt ion gradients

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13
Q

What cell types in tissues are the primary phagocytes of the cellular innate immune system?

A

Macrophages, neutrophils, dendritic cells

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14
Q

What is a respiratory burst?

A

Destruction in phagolysosomes occurs through enzyme degradation, antimicrobial proteins, and toxic effects of reactive oxygen and reactive nitrogen species

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15
Q

What kind of receptors does Dectin 1 bind to?

A

C-type lectin receptors

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16
Q

What kind of receptors does DC-SIGN bind to?

A

C-type lectin receptors

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17
Q

What kind of receptors does SR-A bind to?

A

scavenger receptors

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18
Q

What is an opsonin?

A

an antibody or other substance which binds to foreign microorganisms or cells making them more susceptible to phagocytosis

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19
Q

What opsonin binds to MBL/H-ficolin receptors?

A

carbohydrates

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20
Q

What opsonin binds to C1 receptors (innate system recognition)?

A

LPS (gram negative bacteria)

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21
Q

What opsonin binds to C1 receptors in adaptive system recognition?

A

IgG (antibodies)

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22
Q

What other uses does phagocytosis have in the body?

A
  • act as body’s main scavenger cells

- clear cellular debris, clean up necrotic, apoptotic, or aging cells through identification of DAMP

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23
Q

Describe the role of CD47 and lysophosphatidic acid has in the maintenance of tissues.

A

Apoptotic (dying) cells release lysophophatidic acid (chemoattractant). Healthy cells display CD47 (don’t eat me signal). Cancer cells often overexpress CD47.

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24
Q

What does TLR3/3 recognize and where are they found?

A

Viral dsRNA; found in endosomes/lysosomes

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25
What does TLR4/4 recognize and where are they found?
Viral proteins, gram-negative bacteria; those that bind gram-negative bacteria are found in the plasma membrane and those that bind to viral proteins are found in endosomes/lysosomes
26
What does TLR5/5 recognize and where are they found?
Flagellated bacteria; found in the plasma membrane
27
What does TLR8/8 recognize?
viral ssRNA; found in endosomes/lysosomes
28
What does TLR9/9 recognize and where are they found?
bacterial/viral DNA: found in endosomes/lysosomes
29
What does TLR2/6 recognize and where are they found?
gram-positive bacteria and fungi; found in plasma membrane
30
Critical thinking: Why does it make sense that some TLR pairs look for MAMPs within endosomes and lysosomes, while others look for MAMPs on the cell surface?
Viral danger may lurk inside the cell, because they cannot divide and function if they are outside of the cell.
31
What do CLRs recognize and where would you find them on an innate immune cell?
C-type lectin receptors= heterogenous population of surface PRRs; recognize cell wall components (glucans of bacteria/fungi); trigger same pathway as TLRs (however, variation in the exact genes activated downstream based on inputs); some promote phagocytosis Found on the surface of innate immune cells.
32
What do RLRs recognize and where would you find them on an innate immune cell?
Recognize viral double stranded RNAs found in RNA helicases (inside cells)
33
What do NLRs recognize and where would you find them on an innate immune cell?
NOD-like receptors= cytosolic PRRs (inside cell); activated by intracellular MAMPs, DAMPs, or other harmful substances
34
Which PRRs discussed can also promote phagocytosis?
CLRs
35
For all PRRs discussed in this section, what are the common gene products of receptor signaling?
Interferons, antimicrobials, cytokines, and chemokines
36
What is the etymology of the word “inflammation”?
Inflammation comes from the Latin inflammare, which means” to set on fire”
37
What two primary forms of inflammation are there? Can you give a couple of examples of each?
• Acute= combating infection/damage (short term) o Snake bites, bacterial wound infections • Chronic= infection/damage not resolved (long term) o Rheumatoid arthritis o Crohn’s disease
38
What are the hallmarks of inflammation?
* Redness= rubor * Swelling with heat= tumor cum calore * Pain= dolore
39
Exudate
fluid that leaks from vessels
40
Edema
overall swelling associated with fluid accumulation
41
Chemotaxis
movement in response to chemical signals
42
Extravasation/diapedesis
movement of WBCs out of vessels
43
What are the three primary proinflammatory cytokines produced?
* TNF-a * IL-1 * IL-6
44
Which cells are best known for producing three primary proinflammatory cytokines?
released by resident macrophages, dendritic cells, and mast cells
45
What are two inflammatory mediators produced?
Prostaglandins and histamine are inflammatory mediators released by mast cells
46
What three outcomes occur when endothelial cells of blood vessels bind to proinflammatory cytokines?
three outcomes occur when endothelial cells of blood vessels bind to proinflammatory cytokines? • Vasodilating • Releasing the chemokine IL-8 • Expressing cell adhesion molecules (CAM)
47
What systemic effects are produced from proinflammatory cytokines?
- Fever - Acute Phase Responses - release of WBC from bone marrow
48
Fever
o The proinflammatory cytokines trigger prostaglandin synthesis and release, which acts on the hypothalamus of the brain to cause an increase in body temp  This is protective, as a fever inhibits microbial growth of some pathogens
49
Acute Phase Response
o Increased synthesis/secretion of antimicrobial proteins from the liver  MBL (opsonin)  CRP (opsonin)  Complement components
50
How is inflammation measured clinically?
- measuring CRP levels (opsonin) | - a WBC count blood test
51
Which cytokine enhances activation of NK cells?
IFN-a
52
What cytokines do NK cells secrete and what are the primary effects of these cytokines in the body?
Il-6 and TNF-a(proinflammatory), Type I IFNs (antiviral) and IFN-y (macrophage activator) These cells can selectively kill self cells
53
How do NK cells use activating ligands and MHC I receptor levels to determine whether or not to kill a cell?
Activating receptors that bind cell surface ligands that indicate “bad” cells Inhibiting receptors that recognize surface proteins common to healthy cells (MHC proteins)
54
What proteins do NK cells use to trigger lysis or apoptosis in their targets?
- Perforins=punch holes in membranes | - Granzymes= trigger apoptosis
55
What importance does the NK cell receptor CD16 play in improving NK cell responses?
NK cells get even better after an adaptive immune response has been mounted • They use CD16 receptors to target cells bound by antibody • Cross-linking of CD16 triggers degranulation into a lytic synapse
56
Would NK cells be more effective against a viral pathogen during a primary or secondary response?
secondary response because of the CD16 response
57
What two primary categories of defects can affect inflammatory responses exist?
* Defects that prevent adequate production of proinflammatory mediators can increase susceptibility to infections * Defects that prevent adequate anti-inflammatory mediators can cause inflammatory disorders
58
What is an example of a positive feedback mechanism for inflammation?
o Cellular responses to proinflammatory cytokines IL-1 and TNF-a include production of more of these cytokines o Activate similar pathways that MAMP or DAMP binding do o Is great for initial stages of infection, because it allows a strong response with limited cells
59
What is an example of a negative feedback mechanism for inflammation?
o Production of soluble decoy receptors for IL-1 and TNF-a occurs after their production that bind to and inhibit their effects o The anti-inflammatory cytokine IL-10 is produced following initial activation of inflammation o Is great for dulling a response that has already started
60
Pathogen avoidance by avoiding detection by PRRs
Several viruses (ebola, influenza, vaccinia) encode proteins that bind cytosolic viral dsRNA and prevent it from binding and activating RLR.
61
pathogen avoidance by blocking PRR signaling pathways
o West Nile Virus NS1 protein inhibits NF-kB and IRF transport into the nucleus
62
Pathogen avoidance by preventing killing or replication inhibition
o Salmonella and Listeria bacteria rupture the phagosome membrane and escape to the cytosol
63
What innate immune processes are made more specific to a particular antigen threat once adaptive immunity kicks in?
* Bacteriolysis * Opsonization * Antibody-dependent cellular cytotoxicity * Agglutination
64
What three things occur when a dendritic cell binds to a MAMP?
* Increases the expression of MHC II * Increases the expression of T-cell activating coreceptors CD80 and/or CD86 * Increases expression of T-cell activating cytokine profiles
65
How do innate immune dendritic cells control how the adaptive immune system responds to a new antigen?
• The PRR that was activated determines what cytokines the dendritic cell secretes • These cytokines tell naïve T cells which subset to mature to: o TH1  good for intracellular infections o TH17  pro-inflammatory o TH2  Good for strong antibody responses o TREG  Anti-inflammatory
66
What is the purpose of an adjuvant?
The purpose of adjuvants is to improve the immunogenicity of a vaccine that does not have the live pathogen in it. (help to classify antigens ex. Ones that identify viruses)
67
How do adjuvants improve the immunogenicity of vaccines?
1. Extends the presence of antigen in the body (more time = stronger response) 2. Helps APCs recognize & phagocytose antigen (more antigen gets to SLOs) 3. Activates WBCs by triggering PRR binding 4. Activates cytokine/chemokine production for more robust WBC response
68
What are three categories of adjuvants that are used in vaccines?
* Mineral salts * Cells and cytokines * Microbial derivatives

Immunology (17 decks)

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