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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
Q

What does TLR4/4 recognize and where are they found?

A

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

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26
Q

What does TLR5/5 recognize and where are they found?

A

Flagellated bacteria; found in the plasma membrane

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27
Q

What does TLR8/8 recognize?

A

viral ssRNA; found in endosomes/lysosomes

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28
Q

What does TLR9/9 recognize and where are they found?

A

bacterial/viral DNA: found in endosomes/lysosomes

29
Q

What does TLR2/6 recognize and where are they found?

A

gram-positive bacteria and fungi; found in plasma membrane

30
Q

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?

A

Viral danger may lurk inside the cell, because they cannot divide and function if they are outside of the cell.

31
Q

What do CLRs recognize and where would you find them on an innate immune cell?

A

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
Q

What do RLRs recognize and where would you find them on an innate immune cell?

A

Recognize viral double stranded RNAs found in RNA helicases (inside cells)

33
Q

What do NLRs recognize and where would you find them on an innate immune cell?

A

NOD-like receptors= cytosolic PRRs (inside cell); activated by intracellular MAMPs, DAMPs, or other harmful substances

34
Q

Which PRRs discussed can also promote phagocytosis?

A

CLRs

35
Q

For all PRRs discussed in this section, what are the common gene products of receptor signaling?

A

Interferons, antimicrobials, cytokines, and chemokines

36
Q

What is the etymology of the word “inflammation”?

A

Inflammation comes from the Latin inflammare, which means” to set on fire”

37
Q

What two primary forms of inflammation are there? Can you give a couple of examples of each?

A

• 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
Q

What are the hallmarks of inflammation?

A
  • Redness= rubor
  • Swelling with heat= tumor cum calore
  • Pain= dolore
39
Q

Exudate

A

fluid that leaks from vessels

40
Q

Edema

A

overall swelling associated with fluid accumulation

41
Q

Chemotaxis

A

movement in response to chemical signals

42
Q

Extravasation/diapedesis

A

movement of WBCs out of vessels

43
Q

What are the three primary proinflammatory cytokines produced?

A
  • TNF-a
  • IL-1
  • IL-6
44
Q

Which cells are best known for producing three primary proinflammatory cytokines?

A

released by resident macrophages, dendritic cells, and mast cells

45
Q

What are two inflammatory mediators produced?

A

Prostaglandins and histamine are inflammatory mediators released by mast cells

46
Q

What three outcomes occur when endothelial cells of blood vessels bind to proinflammatory cytokines?

A

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
Q

What systemic effects are produced from proinflammatory cytokines?

A
  • Fever
  • Acute Phase Responses
  • release of WBC from bone marrow
48
Q

Fever

A

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
Q

Acute Phase Response

A

o Increased synthesis/secretion of antimicrobial proteins from the liver
 MBL (opsonin)
 CRP (opsonin)
 Complement components

50
Q

How is inflammation measured clinically?

A
  • measuring CRP levels (opsonin)

- a WBC count blood test

51
Q

Which cytokine enhances activation of NK cells?

A

IFN-a

52
Q

What cytokines do NK cells secrete and what are the primary effects of these cytokines in the body?

A

Il-6 and TNF-a(proinflammatory), Type I IFNs (antiviral) and IFN-y (macrophage activator)
These cells can selectively kill self cells

53
Q

How do NK cells use activating ligands and MHC I receptor levels to determine whether or not to kill a cell?

A

Activating receptors that bind cell surface ligands that indicate “bad” cells
Inhibiting receptors that recognize surface proteins common to healthy cells (MHC proteins)

54
Q

What proteins do NK cells use to trigger lysis or apoptosis in their targets?

A
  • Perforins=punch holes in membranes

- Granzymes= trigger apoptosis

55
Q

What importance does the NK cell receptor CD16 play in improving NK cell responses?

A

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
Q

Would NK cells be more effective against a viral pathogen during a primary or secondary response?

A

secondary response because of the CD16 response

57
Q

What two primary categories of defects can affect inflammatory responses exist?

A
  • 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
Q

What is an example of a positive feedback mechanism for inflammation?

A

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
Q

What is an example of a negative feedback mechanism for inflammation?

A

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
Q

Pathogen avoidance by avoiding detection by PRRs

A

Several viruses (ebola, influenza, vaccinia) encode proteins that bind cytosolic viral dsRNA and prevent it from binding and activating RLR.

61
Q

pathogen avoidance by blocking PRR signaling pathways

A

o West Nile Virus NS1 protein inhibits NF-kB and IRF transport into the nucleus

62
Q

Pathogen avoidance by preventing killing or replication inhibition

A

o Salmonella and Listeria bacteria rupture the phagosome membrane and escape to the cytosol

63
Q

What innate immune processes are made more specific to a particular antigen threat once adaptive immunity kicks in?

A
  • Bacteriolysis
  • Opsonization
  • Antibody-dependent cellular cytotoxicity
  • Agglutination
64
Q

What three things occur when a dendritic cell binds to a MAMP?

A
  • 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
Q

How do innate immune dendritic cells control how the adaptive immune system responds to a new antigen?

A

• 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
Q

What is the purpose of an adjuvant?

A

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
Q

How do adjuvants improve the immunogenicity of vaccines?

A
  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
Q

What are three categories of adjuvants that are used in vaccines?

A
  • Mineral salts
  • Cells and cytokines
  • Microbial derivatives

Immunology (17 decks)

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