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Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

Key Concepts associated with innate immunity (6)

A
  • Always on/present
  • Activated rapidly
  • Non-specific
  • Non-adaptive- same on each encounter
  • No clonal expansion
  • No memory cells are generated
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2
Q

Name the Physical barriers of innate immunity (6)

A 
Skin
Mucosal surfaces
Mucociliary escalator
Normal flora
Fever
Eyes
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3
Q

Characteristics of skin that makes it an effective barrier to pathogens (7)

A
  • Intact barrier
  • Sloughing
  • Keratinized cells
  • pH 4 due to sebum
  • Killing of microbes by locally produced Abx (defensins, cathelicidins)
  • Killing of microbes and infected cells by intraepithelial lymphocytes
  • Langerhans cells - if get through intraepithelial
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4
Q

Characteristics of Mucosal surfaces that make it a physical barrier to pathogens

A
  • Covered in mucous

- Mucous contains lactoferrin and lysozyme (breaks down peptidoglycan)

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5
Q

Characteristics of Mucociliary escalator that make it a physical barrier to pathogens

A

Takes things you breathed in (in trachea, upper respiratory tract for example), cilia move it up and then you can swallow it and cough it out or go to acidic stomach

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6
Q

Characteristics of Normal flora that make it a physical barrier to pathogens

A

Prevents binding of pathogens and secrete bacteriocins (toxins against other bacteria)

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7
Q

Characteristics of Fever that make it a physical barrier to pathogens

A

Retards pathogen growth

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8
Q

Characteristics of Eyes that make it a physical barrier

A
  • blinking

- tears have lysozyme

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9
Q

List enzymes and secretions that are part of the innate immune response and how they protect us from pathogens (4).

A
  • Lysozyme
  • Iron-sequestering proteins- transferrin and lactoferrin
  • Antimicrobial peptides/antibiotics (defensins and cathelicidins)
  • Complement
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10
Q

How do lysozymes protect from pathogens?

A
  • Breaks down peptidoglycan (major component of bacterial cell membranes)
  • Present in tears, mucus, and saliva
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11
Q

How do iron sequestering proteins protect us from pathogens?

A

Can bind free iron to create a lack of iron in the blood —> induced hypoferremia
- hide iron from bacteria (many bacteria need iron to survive)

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12
Q

Describe the location of the two iron-sequestering proteins

A
  • Transferrin in blood

- Lactoferrin in mucosal secretions

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13
Q

Name two examples of Antimicrobial peptides/antibiotics

A

Defensins and cathelicidins

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14
Q

Antimicrobial peptides/Abx are found in _______

A

Skin, mucosal secretions, and granules within the phagocytes

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15
Q

Name the two innate complement pathways.

A

Alternative pathway

Lectin pathway

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16
Q

Complement consists of _______ serum proteins

A

> 30

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17
Q

Name the cells that have an important function in their innate immune response.

A

Phagocytes:

  • Neutrophils
  • Macrophages
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18
Q

Mechanisms used by the phagocytes to protect the body from pathogens.

A

Phagocytes (neutrophils and macrophages)- kill via oxidative burst

  • Increased acidity of the vacuole (phagosome) by pumping in H+
  • Phagocyte membrane zips up around the microbe
  • Fusion of the lysosome with the phagosome —> phagolysosome
  • Release of lytic enzymes and ROS and nitrogen molecules (oxidative burst) within the phagolysosome
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19
Q

Neutrophils:

1) Pathogen specific or non-specific?
2) Where are they found?
3) Short or long lived?
4) What do they do?

A

1) Non-specific
2) Blood
3) Short-lived
4) Phagocytosis (Best!)

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20
Q

Macrophages:

1) Pathogen specific or non-specific?
2) Where are they found?
3) Short or long lived?
4) What do they do?

A

1) Non-specific
2) Tissue
3) Short-lived (1-3 days)
4) Phagocytosis and repair and antigen presentation

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21
Q

Name the categories of receptors in the innate immune response.

A 
Toll-like receptors (TLR)
Nucleotide-binding oligomerization domain proteins (NOD)- PRRs
Pentraxins- PRRs
Collectins- PRRs
Ficolins- PRRs
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22
Q

TLRs - give examples

A

Plasma membrane:

TLR1:TLR2- bacterial lipopeptides

TLR2- bacterial peptidoglycan

TLR4- LPS

TLR5- bacterial flagellum

TLR2:TLR6- bacterial lipopeptides

Endosome:

TLR3- dsRNA

TLR7- ssRNA

TLR8- ssRNA

TLR9- CpG DNA

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23
Q

Describe TLRs

A

Different TLRs recognize and bind different PAMPs

Some are on the surface of the cell, some are inside the cell

TLR engagement results in activation of the cell

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24
Q

Describe NODs

A

Nucleotide-binding oligomerization domain proteins (NOD)

Detect microbial PAMPs of pathogens that gain entry inside the cell

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25
Q

Give examples of NODs.

A

NOD-1: ubiquitous in tissues
- recognize peptidoglycan from Gram-negative bacteria

NOD-2: limited to myeloid cells
- recognize a different peptidoglycan motif

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26
Q

Describe Pentraxins

A

Pentraxins are Plasma proteins.

These PRRs recognize a variety of bacterial, fungal, and viral PAMPs

Once bound to the pathogen, they can activate the classical complement pathway

They are produced during the acute phase response- a systemic inflammatory response

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27
Q

Give examples of Pentraxins.

A

C-reactive protein: used as a measure of infection

28
Q

Describe Collectins.

A

Collections are soluble PRRs.

  • Lectins: proteins with a carbohydrate binding domain
  • Common targets such as MANNOSE and FUCOSE are not found in high concentrations on mammalian cells
29
Q

Give some examples of Collectins.

A
  • MBL (Mannose binding lectin): which when bound to mannose on a pathogen, can activate the lectin complement pathway
  • Surfactants A and D are found in alveoli and act as opsonins (something that attaches to pathogen) for alveolar macrophages
30
Q

Describe Ficolins.

A

Ficolins are soluble PRRs.

  • Ficolins have a similar “celery stalk” structure as MBL
  • bind N-acetylglucosamine (in peptidoglycan) or lipoteichoic acid (in gram positive bacteria)
  • when bound to a pathogen, it can also activate the lectin complement pathway
31
Q

List the steps of Extravasation.

A

Rolling
Activation of Integrins
Stable Adhesion
Transendothelial Migration

32
Q

Describe Rolling

A

1) Tissue macrophages detect pathogens or injury —> cytokines secreted
2) Cytokines cause an upregulation of adhesion molecules on the local vascular EC’s
3) Leukocytes (neutrophils/monocytes) drift toward the vessel wall (margination)
4) Rolling of leukocytes is caused by low affinity binding and release of the cells with the newly unregulated adhesion molecules

33
Q

Activation of Integrins

A

The repetitive binding/detaching actions between leukocytes and EC’s results in conformational change of the adhesion molecules on the leukocytes

Once the conformation change has occurred, the leukocytes can bind with greater strength to the adhesion molecules on the vascular EC’s

34
Q

Stable Adhesion

A

Conformational change of vascular adhesion molecules allows for stable binding and arrest of the cells

35
Q

Transendothelial Migration

A

Now that the leukocyte has stopped moving, it undergoes changes to allow it to pass between the vascular EC’s

The cell flattens out along the endothelial surface, then squeezes between the EC’s into the tissues

36
Q

What receptors are associated with Rolling?

A

Selectin ligand on the leukocyte binds to the selectin receptor on the EC surface

37
Q

What receptors are associated with Integrin activation by Chemokines?

A

Proteoglycan bound to a Chemokine on the EC surface binds to the Chemokine receptor on the leukocyte which activates the integrin ligand on the EC surface

38
Q

What receptors are associated with stable adhesion?

A

The Selectins disassociate

The integrins bind the integrin ligands in high-affinity state

Proteoglycan-Chemokine stays bound

39
Q

Steps of Inflammation. (5)

A 
Vasodilation
Phagocyte migration
Increased phagocytosis
Cytokine production
Plasmin remodeling and repair
40
Q

Describe Vasodilation as a part of inflammation

A

Chemokines and cytokines cause vasodilation which allows plasma, cells, and molecules to enter the tissues

41
Q

Describe phagocyte migration as a part of inflammation

A

Extravasation of neutrophils within 30-60 minutes

Extravasation of monocytes in 4-6 hours

42
Q

Describe phagocytosis as a part of Inflammation

A

Macrophages, DCs, and recruited leukocytes increase their phagocytic activity

43
Q

Describe cytokine production as a part of Inflammation.

A

Pro-inflammatory cytokines (IL-1, IL-6, and TNF-alpha) are produced by the activated tissue macrophages —> upregulation of adhesion molecules on vascular ECs

44
Q

Name the cytokines associated with inflammation.

A

IL-1
IL-6
TNF-alpha

45
Q

Define inflammation.

A

VD and increased vascular permeability occur as a result of cytokines, kinins, and histamine released by cells at the site of infection (recognized when PRR binds PAMP) or due to tissue injury

46
Q

What is the acute phase response?

A

Systemic response that results from the cytokines entering the bloodstream and reaching distant sites

47
Q

Describe 3 features of the Acute phase response

A

1) Fever
2) Hematopoiesis to replace the monocytes, neutrophils and complement proteins that have left the circulation
3) Sequestration of iron into the liver- induced hypoferremia

48
Q

Inflammation timeline with cells:

  • PRRs
  • Macrophages
  • Mast cells
  • Cytokines
  • PMNs
  • Monocytes
A
  • Tissue injury or pathogen recognition (PRR binds PAMP)
  • Macrophages are activated and secrete pro-Inflammatory cytokines (IL-1,IL-6,TNF-alpha)
  • Mast cells release histamine
  • Cytokines and histamine act on vascular EC’s resulting in VD
  • leakage of plasma fluid and proteins into tissue (tumor)
  • Extravasation of neutrophils in about 30 mins
  • Extravasation of monocytes —> macrophages (in about 4 hours) —> more cytokines
  • Pathogens are phagocytosed and killed!!
  • Repair
49
Q

Describe bystander tissue damage

A

Result of inflammation

External release of enzymes by PMNs and macrophages can cause tissue damage to nearby tissues

Granule contents can also stimulate nerves, leading to pain (dolor)

50
Q

Describe cytokines and processes involved in the Acute phase response

A

IL-1, IL-6, and TNF fo to he hypothalamus to “reset” body temperature = fever

IL-1 and IL-6 go to the liver to increase production of acute phase proteins (CRP, MBL, PTX3, SAP)

IL-1, IL-6, and TNF go to the bone marrow to increase Hematopoiesis (to replace neutrophils)

51
Q

List 2 clinical findings seen with the Acute Phase Response.

A 
Fever
Induced Hypoferremia (for bacterial infections)
52
Q

Clinical Correlation: Mutations in Nod2 has been correlated with an increase in the susceptibility of _______

A

Crohn’s disease

53
Q

Acute Phase Proteins:

Pentraxins

A

Bind Cla and activate the Classical complement pathway

55
Q

Acute Phase Proteins:

Pentraxins- Serum Amyloid Protein

A

SAP binds to components on bacterial cell walls

56
Q

Acute Phase Proteins:

Pentraxins- Pentraxin 3

A

PTX3 binds various molecules on bacteria, fungi and viruses

57
Q

Acute Phase Proteins:

Collectins

A

Contains lectin (a protein that binds carbohydrate)

58
Q

Acute Phase Proteins:

Collectins- Mannose Binding Lectin

A

MBL binds mannose sugars on bacterial and yeast surfaces, activating lectin pathway

59
Q

Acute Phase Proteins:

Collectins- Surfactant Proteins A and D

A

SP-A and SP-D: found in alveoli

60
Q

Acute Phase Proteins:

Ficolins

A

Similar structure to MBL

Bind N-acetylglucosamine of bacterial cell walls and lipoteichoic acid of Gram + cell walls

Can activate the Lectin pathway

61
Q

Acute Phase Proteins:

Pentraxins- C-reactive protein

A

CRP binds to components on bacterial and fungal cell walls and is a bio marker of inflammation, can increase 1000 fold during infection

62
Q

What bactericidal enzyme is found in saliva?

A

Lysozyme

63
Q

T/F: The mucosal layer is not as effective as a barrier as the skin.

A

True

64
Q

PAMP

A

Pathogen-associated molecular patterns

Common motifs/patterns present on pathogens recognized by cells

65
Q

PRR

A

Pattern recognition receptors

For innate cells, these receptors are not specific to an antigen

Bind PRR’s

66
Q

What are the different types of innate immunity? (3)

A

1) Phagocytosis/opsonization
2) Production of Antimicrobial peptides, toxic ROS, and Nitrogen species
3) Physical barriers

67
Q

What is the role of inflammation? (3)

A

1) Deliver immune cells and effector molecules (ex. Complement) to the site of the infection or injury
- macrophages secrete cytokines and complement proteins.
- cytokines: chemical trail for neutrophils and monocytes to follow

2) Remove or limit the spread of the injurious agent
3) Repair tissue and clean up damage

Immunology (6 decks)

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