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SMP - MIM Part 1 > Lecture 8 - Innate Immunity > Flashcards

Lecture 8 - Innate Immunity Flashcards

1
Q

Why does the innate immunity have potential for collateral damage?

A

Because it has low specificity so self can be mistaken with an antigen

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2
Q

Do plants and invertebrates have an adaptive immunity?

A

NOPE

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3
Q

What is activation of the innate immune response a prereq for in vertebrate?

A

Prereq for induction of acquired adaptive immunity

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4
Q

Why is the innate immune response so quick?

A

Because it uses products of germ-line genes

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5
Q

What are the 4 stages of a response to an infection?

A
  1. Infectious agent adhere to the epithelial cells and then cross the epithelium
  2. Local infection of epithelium
  3. Local infection of tissues
  4. Adaptive immunity
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6
Q

Protection from stage 1 of infection?

A

Immune exclusion to protect pathogens from adhering to and colonizing skin and mucosal barriers

Conducted by:

  1. Normal flora
  2. Local chemical factors
  3. Phagocytes (esp. in lungs): MOs, DCs, and immune lymphoid cells
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7
Q

Protection from stage 2 of infection?

A

Local immune response may prevent the infection from becoming established

Conducted by:

  1. Wound healing mechanism
  2. Antimicrobial proteins and peptides
  3. Phagocytes: MOs, DCs, and immune lymphoid cells
  4. Complement system
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8
Q

Protection from stage 3 of infection?

A

Helps to contain the infection and also delivers the infectious agent, carried in lymph and inside dendritic cells, to local lymph nodes => sound the alarm

Conducted by:

  1. Complement system
  2. Cytokines
  3. Chemokines
  4. Stress proteins
  5. Phagocytes
  6. NK cells
  7. MOs
  8. DCs
  9. Blood clotting to limit spread
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9
Q

Protection in stage 4 of infection?

A

Control initiation and type of adaptive immunity and turn it off when it’s done its job

Conducted by:

  1. Specific ABs
  2. Cytotoxic T cells
  3. MOs activated by T-cells
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10
Q

Do all pathogens need to adhere to the epithelium to infect?

A

YES - except for 2 types:

  1. Pathogens that use an intermediate vector: tick-borne diseases or mosquito-borne diseases where the pathogen uses a bite to enter
  2. Bacteria that produce potent exotoxins (e.g. Clostridium botulinum produces botulinum toxin)
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11
Q

Is the barrier epithelium thick?

  1. Skin
  2. Mucosae
A
  1. Yes

2. No (sometimes 1 cell thick)

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12
Q

Is the barrier epithelium impermeable?

  1. Skin
  2. Mucosae
A
  1. Yes

2. No

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13
Q

Does the barrier epithelium desquamate?

  1. Skin
  2. Mucosae
A
  1. Yes

2. Yes

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14
Q

What does the barrier epithelium secrete?

  1. Skin
  2. Mucosae
A
  1. Sweat

2. Tears, saliva, milk, respiratory secretions, GI secretions, GU secretions

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15
Q

Why is desquamation of barrier epithelia important?

A

The continuous shedding of squames carries away microorganisms that have adhered to them

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16
Q

Do the secretions flow?

  1. Skin
  2. Mucosae
A
  1. No

2. Yes

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17
Q

What 3 components do the secretions of both the skin and mucosae contain?

A
  1. Soluble antimicrobial factors
  2. PPRs
  3. Endogenous microbiota
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18
Q

Describe the soluble antimicrobial factors in the secretions of both the skin and mucosae? What to note?

A

Predominantly proteins but can be fatty acids in the case of skin, with some being families of:

  1. Highly cationic proteins such as histatins and defensins which function to create channels in the microbial cell membrane
  2. Metal-sequestering proteins like lactoferrin and enzymes that create reactive oxygen intermediates such as lactoperoxidase.

Note: many of these immune factors are found in the lysosomal vacuoles of professional phagocytes and dendritic cells, also

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19
Q

5 functions of the normal microbiota of barrier epithelia?

A
  1. COMPETITION FOR NUTRIENTS
  2. COMPETITION FOR RECEPTORS
  3. PRODUCTION OF ANTAGONISTS (e.g. hydrogen peroxide and bacteriocins)
  4. MAINTENANCE OF LOW BUT CONSTANT EXPRESSION OF MHC II ON MACROPHAGES AND OTHER APC
  5. STIMULATION OF CROSS-PROTECTIVE ANTIBODIES
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20
Q

2 other names for the normal microbiota of barrier epithelia?

A

Endogenous or commensal microbiota

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21
Q

What happens if the normal microbiota of barrier epithelia is disrupted? How can this occur?

A

Exogenous microorganisms can establish on the epithelial surfaces and can be resistant to anti-bacterial antibiotics

By the used of broad spectrum antibiotics

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22
Q

How does the normal microbiota stimulate cross-protective ABs? Examples?

A

They may share epitopes with virulence factors of external pathogens so antibodies induce against these resident bacteria may offer some protection against pathogens that share antigens with resident bacteria

Examples:

  1. Inside the uterus the fetus is sterile but as it passes down the birth canal and enters the outside world it become colonized by bacteria that eventually constitute the resident microbiota => antigens of these bacteria, particularly lipopolysaccharide, are important in driving the development of the immune system
  2. Capsule of E. Coli identical to capsule of N. Meningitis
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23
Q

Are there more microorganisms colonizing the skin and mucosal surfaces or somatic cells?

A

10-100 x more microorganisms

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24
Q

What molecules are upregulated/released when there is epithelial damage?

A
  1. Cytokines/chemokynes
  2. Stress proteins
  3. Components of dead/dying or alive microorganisms
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25
Q

2 types of SIGNALING PPRs?

A
  1. Transmembrane

2. Cytosolic

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26
Q

Where are transmembrane signaling PPRs found?

A
  1. Cell surface

2. Phagosome/lysosome membrane

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27
Q

2 types of transmembrane PPRs? On which cells is each found?

A
  1. Toll-like receptors: polymorphonuclear cells, DCs, MOs, monocytes, B and T cells, NKs and somatic cells)
  2. C-type lectins
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28
Q

How many types of TLRs in humans?

A

10

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29
Q

How do C-type lectins work?

A
  1. Co-operate with TLRs
  2. Signal on their own
  3. Some are endocytic on phagocytes
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30
Q

What is the family of cytosolic signaling PPRs? What do they sense?

A

Nucleotide oligomerization domain-like receptor (NLR) family that sense RNA and DNA from pathogens and different wall structures

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31
Q

Purpose of signaling PPRs?

A

Inform the body regarding:

  1. Nature i.e., bacterium, fungus, virus, etc. of the pathogen
  2. Size of the pathogen
  3. Infectious dose of pathogen

to instruct adaptive immunity on what type of adaptive response i.e., antibody and/or effector T cells is required to most effectively combat it

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32
Q

5 examples of NLR signaling PPRs?

A
  1. NOD1 - NOD5 & CIITA (diaminopimilic acid - muramyldipeptide)
  2. ISD SENSOR (DNA)
  3. RIG-1/MDA5 (RNA helicases) sense viral RNA
  4. NALP1 - 14 (LPS, pore-forming toxins; type III and IV bacterial secretion systems)
  5. NALP3 INVOLVED IN FORMATION & ACTIVATION OF INFLAMMASOMES, promoting the maturation of inflammatorycytokine IL1β & IL-18
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33
Q

What do PAMPs have in common?

A

Structural elements of pathogens that are not easily mutable because mutation may be lethal

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34
Q

TLR1:TLR2 ligand?

A

Lipopeptides and GPI anchors

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35
Q

TLR1:TLR2 microorganism recognized?

A

Bacteria and parasites

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36
Q

TLR1:TLR2 and TLR2:TLR6 heterodimers: 5 cells carrying them?

A
  1. Monocytes
  2. DCs
  3. Eosinophils
  4. Basophils
  5. Mast cells
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37
Q

TLR1:TLR2 and TLR2:TLR6 heterodimers: cellular location?

A

Plasma membrane

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38
Q

TLR3 ligand?

A

Double-stranded viral RNA

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39
Q

TLR3 microorganism recognized?

A

Viruses

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40
Q

Cells carrying TLR3?

A

NKCs

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41
Q

Cellular location of TLR3?

A

Endosomes

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42
Q

Ligand of TLR4:TLR4 homodimer?

A

Lipopolysaccharide

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43
Q

TLR4:TLR4 homodimer microorganisms recognized?

A

Gram (-) bacteria

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44
Q

TLR4:TLR4 homodimer: 4 cells carrying it?

A
  1. Macrophages
  2. DCs
  3. Mast cells
  4. Eosinophils
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45
Q

TLR4:TLR4 homodimer: cellular location?

A

Plasma membrane

46
Q

TLR5: ligand?

47
Q

TLR5: microorganisms recognized?

A

Motile bacteria with a flagellum

48
Q

Cells carrying TLR5?

A

Intestinal epithelial cells

49
Q

Cellular location of TLR5?

A

Plasma membrane

50
Q

TLR7: ligand?

A

Single-stranded viral RNAs

51
Q

TLR7: microorganisms recognized?

52
Q

4 cells carrying TLR7?

A
  1. Plasmacytoid DCs
  2. NKCs
  3. Eosinophils
  4. B cells
53
Q

Cellular location of TLR7?

54
Q

TLR8: ligand?

A

Single-stranded viral RNAs

55
Q

TLR8: microorganisms recognized?

56
Q

Cells carrying TLR8?

57
Q

Cellular location of TLR8?

58
Q

TLR9: ligand?

A

Unmethylated CpG-rich DNA

59
Q

TLR9: microorganisms recognized?

A

Bacteria and viruses

60
Q

4 cells carrying TLR9?

A
  1. Plasmacytoid DCs
  2. B cells
  3. Eosinophils
  4. Basophils
61
Q

Cellular location of TLR9?

62
Q

Ligand and microorganisms recognized by TLR10 homodimer and heterodimer with TLR1 and 2?

63
Q

4 cells carrying TLR10 homodimer and heterodimer with TLR1 and 2?

A
  1. Plasmacytoid DCs
  2. B cells
  3. Eosinophils
  4. Basophils
64
Q

Cellular location of TLR10 homodimer and heterodimer with TLR1 and 2?

65
Q

TLR2:TLR6 2 ligands?

A
  1. Lipoteichoic acid

2. Zymosan

66
Q

TLR2:TLR6 2 microorganisms recognized?

A
  1. Gram (+) bacteria

2. Yeasts (fungi)

67
Q

What is the only TLR so far for which a direct interaction with a microbial product?

A

TLR5: flagellum

68
Q

6 outcomes of signaling PPR ligation of PAMPs?

A
  1. RELEASE OF PRO-INFLAMMATORY CYTOKINES by DCs and macrophages => vasodilation to recruit neutrophils to the site of infection
  2. UPREGULATION OF CHEMOKINE RECEPTOR CCR7 => allows attraction by CCL19 & CC721 produced by lymph nodes for DCs to migrate there
  3. SECRETION OF CCL18 => ATTRACTs NAÏVE T CELLS
  4. UPREGULATION/EXPRESSION OF MHC I & MHC II
  5. UPREGULATION/EXPRESSION OF CO-STIMULATORY MOLECULES
  6. UPREGULATION/EXPRESSION OF CELL ADHESION MOLECULES
69
Q

What does polarization of the adaptive immune system refer to?

A
  1. Directing T cells to follow TH17, TH1 or TH2 pathways

2. Activation of B cells

70
Q

What are mature conventional DCs?

A

DCs that are primarily concerned with the activation of naive T cells and express MHC proteins and co-stimulatory molecules for priming naive T cells when they are mature

71
Q

What are plasmacytoid DCs? Where are they found?

A

Subset of conventional dendritic cells that cannot process antigen efficiently, found in the LNs but:

  1. Express TLR-7 and 9 to recognize viruses
  2. Secrete IFNα and IFNβ => activate NKCs
  3. Express CD40 L which interacts with CD40 on conventional DCs to help sustain IL-12 production => TH1 activation
72
Q

Describe immature conventional DCs.

A

Lack many of the cell-surface molecules of mature DCs, but have numerous surface receptors that recognize pathogen molecules, including most of the TLRs

73
Q

What are the 4 determinations made by PPRs and the adaptive checkpoint controlled by each?

A
  1. Discriminate between self, and innocuous non-self that do not require activation of adaptive immunity and dangerous non-self which probably does
  2. Determine class of infection: whether the pathogen is extracellular (engages membrane and endocytic/phagocytic PRRs) or intracellular (engages cytosolic PRRs) and whether the pathogen is a bacterium, virus, etc., by the types of PRRs engaged by the PAMPs so that the appropriate type of adaptive response can be brought to bear on the pathogen
  3. Determine level of infection: number of PRRs ligated and the duration of ligation to determine the magnitude and the duration of the adaptive immune response necessary
  4. Determine whether the infection warrants immediate vs future defense, i.e. the creation of effector vs memory T and B cells
74
Q

2 types of endocytic PPRs?

A
  1. Transmembrane

2. Soluble (act as opsonins)

75
Q

4 types of endocytic transmembrane PPRs?

A
  1. C-type lectin family
  2. Scavenger receptor family
  3. N-formyl met receptors
  4. Complement receptors
76
Q

4 C-type lectin endocytic PPRs?

A
  1. DECTIN-1 (β1-3 glucan)
  2. DC-SIGN (asialoglycoproteins)
  3. MANNOSE RECEPTOR
  4. GLUCAN RECEPTOR
77
Q

Describe the scavenger receptor family of endocytic PPRs?

A

PPRs that recognize negatively charged macromolecules, including:

  1. Oxidized low-density lipoproteins
  2. Damaged or apoptotic cells
  3. Pathogenic microorganisms
78
Q

What do N-formyl met receptors recognize?

A

Bacterial proteins

79
Q

2 examples of N-formyl met receptors?

A
  1. FPR

2. FPRL-1

80
Q

4 types of soluble endocytic PPRs?

A
  1. MANNOSE-BINDING LECTIN
  2. C-REACTIVE PROTEIN: PHOSPHORYLCHOLINE/PHOSPHATIDYLETHANOLAMINE
  3. LUNG SURFACTANT PROTEINS: SP-A & SP-D HAVE CARBOHYDRATE RECOGNITION DOMAINS
  4. COMPLEMENT COMPONENTS: C3b, C4b
81
Q

Describe the 8 steps of phagocytosis for leading onto MHC II molecules?

A
  1. Chemotaxis: of phagocytic cell to the site of infection by recognizing graded chemokines being secreted by damaged epithelium or PAMPs
  2. Attachment: pathogen is up-taken usually following opsonization by C3b and/or IgG or, indirectly, by the soluble PPRs such as C-reactive protein
  3. Phagocytosis: membrane of the professional phagocyte extend pseudopods by rearrangement of the actin cytoskeleton and envelopes the pathogen in a tight vesicle formed from the invaginated cell membrane OR pathogen simply sinks in
  4. Spare cell membrane is returned to be once again incorporated into the membrane.
  5. The phagosome moves towards the center of the cell and during its journey its content becomes increasingly acidic and its composition changes because portions of its membrane containing receptors traffic back to the surface while endosomes fuse with it emptying their cargo into it
  6. Vacuole formation: as the phagosome reaches the center of the cell it fuses with several lysosomes that contain antimicrobial factors and acid proteases to form a phagolysosome => oxygen independent pathway
  7. Multicomponent NADPH oxidase and NO synthase are assembled in the membrane of the phagolyosome and the phagocyte takes up oxygen (the respiratory burst) to enable the NADPH oxidase to create several reactive oxygen intermediates/species and reactive nitrogen intermediates (both antimicrobial)
  8. Killing: within the phagolysosome acid proteases hydrolyze microorganism proteins into peptides suitable for loading into the grove of MHC II molecules
  9. Once loaded with pathogen-derived peptides the MHC II molecules traffic to the cell membrane where they present the MHCII peptide complex to CD4 T cells => induction of adaptive immunity
82
Q

3 aims of phagocytosis?

A
  1. Kill the pathogen
  2. Load pathogen peptides generated in the phagolysosome onto MHC II molecules which traffic to the cell membrane to be presented to CD4 helper T cells
  3. Release cytokines and chemokines that recruit reinforcements from the blood to the site of infection and to active lymphocytes
83
Q

Difference between endosome and phagosome?

A

Phagocytic vesicle is termed an endosome or, if the content is a microorganism, a phagosome

84
Q

2 effects of decreasing pH of the phagosome?

A
  1. Could directly kill the pathogen

2. Activates proteases to break down the pathogen

85
Q

Which is more important during phagocytosis: oxygen dependent or oxygen independent pathway?

A

Oxygen dependent

86
Q

What do activated macrophages secrete? AKA what the the 5 pro-inflammatory cytokines? What are their systemic effects?

A

5 cytokines:

  1. IL-1β
  2. TNF-α
  3. IL-6
  4. CXCL8
  5. IL-12

Systemic: hypothalamus for fever and liver for complement elements

87
Q

Main role of IL-1β?

A

Activates vascular endothelium

88
Q

Main role of TNF-α?

A

Activates vascular endothelium and increases vascular permeability => increased entry of IgG, complement, and cells to tissues + increased fluid drainage to LNs

89
Q

2 roles of IL-6?

A
  1. Lymphocyte activation

2. Increased AB production

90
Q

Role of CXCL8?

A

Chemotactic factor that recruits neutrophils, basophils, and T cells to the site of infection

91
Q

2 roles of IL-12?

A
  1. Activates NKCs

2. Induces the differentiation of CD4 T cells into TH1 cells for them to make IFN-gamma

92
Q

Most important immune cell in acute inflammation?

A

Polymorphonuclear leukocytes

93
Q

Where are mast cells located?

A

Strategically located below the barrier epithelia and around small blood vessels and nerves

Mast cells release

94
Q

What stimulates mast cells to degranulate?

A
  1. Direct injury

2. Activated complement components

95
Q

What do mast cells release during degranulation? Purpose of each? Which 2 are released from the preformed granules (vs being synthesized upon activation)?

A
  1. ***Enzymes: tryptase, chymase, cathepsin G, carboxypeptidase => remodel connective tissue matrix
  2. ***Toxic mediators: histamine, heparin => toxic to parasites, increase vascular permeability, SM contractions, anticoagulation
  3. Cytokines: IL-13 and IL-4 (TH2 polarization) + IL-3, IL-13, GM-CSF (eosinophil production and activation)
  4. Chemokines: CCL3 => attracts macrophages, monocytes, and neutrophils
  5. Lipid mediators: prostaglandins D2, E2, leukotrienes C4, D4, E4 (SM contractions, chemotaxis of eosinophils, basophils, TH2, vascular permeability, mucus secretions, bronchoconstriction) + platelet activating factor (attract leukocytes, amplify production of lipid mediators, and activate neutrophils, eosiniphils, and platelets)
96
Q

Describe the process by which monocytes facilitate the emigration of neutrophils from blood vessels.

A
  1. Monocytes leave the vasculature to enter the connective tissue and patrol as wandering macrophages or dendritic cells
  2. To enable cells to leave the blood vessels receptor-ligand interactions must occur between cell adhesion molecules on both the endothelium and cellular elements in the blood
    3a. Under ‘resting’ conditions selectins bind to sugars that terminate adhesion molecules on the surface of leukocytes (e.g. sialylated form of the LewisX blood group antigen) => allows leukocyte to roll along the endothelium
    3b. Under the influence of cytokines and chemokines cell adhesion molecules on the surface of the endothelium and the leukocyte are up-regulated
  3. Tight binding between leukocyte and endothelium
  4. Diapedesis between endothelial cells
  5. Migration toward infection site by following cytokine gradient
97
Q

3 families of cell adhesion molecules? Describe each. What 2 bind to each other?

A
  1. Selectins: bind carbs and are present on endothelium platelets
  2. ***Integrins: present on leukocytes
  3. ***ICAMs (InterCellular Adhesion Molecules): present on both the endothelium and leukocytes
98
Q

How does vasodilation facilitate adhesion of leukocytes on the endothelium?

A

Flow rate is decreased

99
Q

What cytokines have some whole body effects? What are these?

A

IL-1, IL-6 and TNF-α can act on remote organs similar to hormones

  1. Liver: acute phase protein synthesis (C-reactive protein, mannone-binding lectin) => activation of complement + opsonization
  2. Bone marrow: neutrophil mobilization => phagocytosis
  3. Hypothalamus: increased body temp
  4. Fat/muscle: protein and energy mobilization to allow increased body temp
  5. DCs: TNF-α stimulates dendritic cells to seed the draining lymph nodes where they become dedicated APCs => initiation of adaptive immune response
100
Q

What happens if the cytokine demand placed on the bone marrow is high?

A

Immature neutrophils termed ‘band forms’ are released into the blood

101
Q

3 effects of fever during the acute phase immune response?

A
  1. Decreased viral and bacterial replication
  2. Increased antigen processing
  3. Increased specific immune response
102
Q

What are 5 types of acute phase proteins released mainly by the liver in response to certain cytokines? List examples for each.

A
  1. Major: serum amyloid A and P, C-reactive protein
  2. Complement components: C2, C3, C4, C5, C9, B, C1-inhibito, C4 binding protein
  3. Coagulation proteins: fibrinogen, von Willebrand factor
  4. Protease inhibitors: α1-anti trypsin, α1-antichymotrypsin, α2-anti-plasmin
  5. Metal-binding proteins: haptoglobin, haemopexin, ceruloplasmin, MnSod
103
Q

Purpose of metal-binding proteins during the acute phase response?

A

Bacteria have a requirement for metal ions

104
Q

4 roles of interferons in the acute phase response? What cells secrete these?

A

Triggered by cytosolic PRR ligation of double-stranded RNA all nucleated cells secrete IFNα and IFNβ

  1. They shut down viral replication => destroys both the virus and infected host cells
  2. In non-immune nucleated cells IFNα and IFNβ increase expression of MHC I to better display pathogen peptides
  3. In immune cells both MHC I and MHC II are up-regulated
  4. Activate NKCs to kill virally-infected cells
105
Q

How do shut down viral replication?

A
  1. By inducing the cell to produce large amounts of protein kinase R(PKR) which phosphorylates eLF2in response to new viral infections (translation initiation factor that forms an inactive complex with another protein, calledeLF2B, to reduce protein synthesis within the cell)
  2. RNAse L, also induced following PKR activation, destroys RNA within the cells to further reduce protein synthesis of both viral and host genes
106
Q

2 other names for NKCs? Why?

A

Large granular lymphocyte or a null cell because it doesn’t express CD3, CD4, CD8 or the TCR

107
Q

Why are NKCs considered innate immune cells?

A

Because its interaction with cells expressing MHC I is NOT dependent on the peptide they present, but rather depends on the density of MHC I on the cell surface

108
Q

How does the NKC work?

A

It has several inhibitory and activating receptors on its surface and surveys the surface of nucleated cells looking for cells that have a reduce density or altered MHC I

  1. When an NK cell docks with a healthy cell expressing normal levels of MHC I its inhibitory receptors, KIR 20, KIR30 and the heterodimer CD94/NKG2 engage MHC I and prevent NK cell activation
  2. If an NK cell docks with a virus-infected or cancerous cell in which MHC I has been down-regulated the NK inhibitory receptors cannot exert their suppressive signals and activating receptors are activated => NK cell is activated to kill the target cell using the same mechanisms as the cytotoxic CD8 T cell, that is, perforin and granzymes
109
Q

What 2 immune cells can kill virus infected cells? Why do we need 2?

A
  1. Cytotoxic T cells
  2. NKCs

Need for 2: cytotoxic T cells need to recognize peptides on MHC I (MHC restricted) but a lot of viruses downregulate MHC I expression

110
Q

What KIR stand for?

A

Killer inhibitory receptor

SMP - MIM Part 1 (14 decks)

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