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MS1 - Invaders and Defenders aka Clusterfuck > Week 1 > Flashcards

Week 1 Flashcards

1
Q

_______ and _______ on the surface of bacteria can activate the alternative complement pathway.

A

Peptidoglycans and lipopolysaccharide activate alternative complement

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2
Q

What activates the lectin complement pathway?

A

Oligosaccharides like mannose, fucose, N-acetylglucosamine on bacterial cell surfaces.

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3
Q

How do bacteria resist phagocytosis?

A

They make polysaccharide-rich capsules that make it hard for phagocytes to eat them.

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4
Q

What do bacteria do to prevent activation of the complement cascade?

A

Sialic acid residues on their surface inhibit complement activation

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5
Q

What function does coagulase have for bacteria?

A

Coagulase results in fibrin deposition on the surface of bacteria for a disguise.

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6
Q

What do the bacterial Proteins A and G do, and which bacteria make them?

A

These proteins inhibit the Fc portion of antibodies to prevent recognition by phagocytes. S. aureus makes Protein A and S. pyogenes makes Protein G.

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7
Q

Intracellular bacteria, fungi, and viruses stimulate DCs and NK cells to produce _____, stimulating CD4+ T cell terminal differentiation into _____ cells that go on to make the cytokine ______, which then activates 3 cell types. What are they and what do they do?

A

DCs, NK cells make IL-12 –> CD4+ cells differentiate into TH1 cells that make IFN-gamma –> activation of more NK cells, CD8+ cells, and macrophages –> macrophages make IL-12 that further activates NK cells and promotes TH1 differentiation –> positive feedback loop!

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8
Q

When macrophages are activated by IFN-gamma, what happens to them?

A
  1. Increased antigen processing and presentation.
  2. Increased cytokine production.
  3. Increased inflammatory mediator production.
  4. Increased antimicrobial activity.
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9
Q

Which cytokines to macrophages make?

A

IL-1, IL-6, TNF-alpha

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10
Q

In which organ do B cells develop?

A

Bone marrow

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11
Q

In which organ to T cells develop?

A

Thymus

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12
Q

Name the secondary lymphoid organs.

A
  1. Spleen
  2. Lymphatics
  3. Tonsils/adenoids
  4. MALT
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13
Q

Name three types of antigen presenting cells.

A
  1. Macrophages
  2. Dendritic cells
  3. B lymphocytes
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14
Q

Exogenous antigens are endocytosed by antigen-presenting cells, and subsequently cut up by proteasomes, and put on ______ molecules for presentation to cells of the adaptive immune system.

A

Exogenous antigens are presented on MHC II molecules.

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15
Q

On which MHC class are endogenous (made inside the cell) antigens presented?

A

MHC I

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16
Q

What is an epithelioid cell?

A

A macrophage in a granuloma that looks like an epithelial cell!

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17
Q

Why are granulomas surrounded by a fibrous wall?

A

Macrophages in the granuloma stimulate fibroblasts to make collagen to contain the infection.

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18
Q

What is sarcoidosis?

A

A condition characterized by collections of granulomas in multiple organs.

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19
Q

What do type 1 interferons do? Which cells make them?

A

Type 1 IFNs include IFN-alpha and IFN-beta and they stimulate macrophages and NK cells to produce anti-viral proteins.

Type 1 IFNs are made by lymphocytes and macrophages, among some other cell types.

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20
Q

Which naive T cell type is activated by MHC class I antigen presentation? What about class II MHC? Is this all that is needed for activation?

A

CD8+ T cells bind to MHC I.

CD4+ T cells bind to MHC II.

You also need co-stimulation by CD40 (on the APC) - CD40 ligand (on the T cell) or by B7 (on the APC) - CD28 (on the T-cell)

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21
Q

Can fungi and parasites live either intracellularly or extracellularly?

A

Yeah!

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22
Q

Describe the immune response to extracellular fungi, including which cells are activated and which cytokines are involved.

A

Extracellular fungi result in CD4+ cell differentiation to TH17 cells that make IL-17 –> activation of neutrophils and epithelial cells, especially mucosal epithelial cells

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23
Q

Helminth worms and allergens stimulate CD4+ cell differentiation into _____ cells that produce which cytokines? What do those cytokines do?

A

Helminth worms, allergens –> TH2 cells –> IL-5 activates eosinophils and IL-4 & IL-13 tell B cells to make IgE and IgG4

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24
Q

Name two things that fungi express that can be recognized by PRRs like C-type lectin receptors and TLRs.

A

Polysaccharides mannan and beta-glucan

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25
Q

Does histamine kill parasites?

A

Yeah

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26
Q

What is IL-10?

A

The inhibitory cytokine that turns off the immune response!

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27
Q

What is the mnemonic for remembering the relative proportions of leukocytes in peripheral blood? What are the relative percentages?

A

Never Let Monkeys Eat Bananas

Neutrophils: 60%
Lymphocytes: 30%
Monocytes: 6%
Eosinophils: 3%
Basophils: 1%
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28
Q

What are platelets derived from?

A

Megakaryocytes

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29
Q

What is a bacterial cell wall made mostly out of? How does one differentiate between bacteria that have a thin cell wall with an additional thick, outer membrane, and bacteria that have a thick cell wall with no additional outer membrane?

A

Cell wall is made out of peptidoglycan.

Gram positive bacteria are the ones with thick cell walls and without the additional outer membrane.

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30
Q

Do Gram-positive bacteria have lipopolysaccharide on their surfaces?

A

Nope

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31
Q

Is LPS an endotoxin? Is it a PAMP?

A

Yeah, yeah

32
Q

Which two cell types are the primary TNF-alpha producers?

A

Mast cells, macrophages

33
Q

What does TNF-alpha do?

A

Stimulates everyone to increase expression of chemokines, inflammatory mediators, and adhesion molecules.

34
Q

What do techoic acid residues on gram positive bacterial cell walls do?

A

They provide rigidity to the cell wall by attracting cations like sodium, and magnesium.

35
Q

Can LPS induce fever and depress blood pressure?

A

Yeah

36
Q

Salmonella uses a Type III secretion system to inject ______ into host cells.

A

toxins

37
Q

What is a unicellular fungi called?

What is a multicellular fungi called?

A

Unicellular = yeast

Multicellular = mold

38
Q

The major membrane sterol in fungi is…?

A

ergosterol

39
Q

Describe the structure of a mold. Describe the two subtypes of this structure.

A

Mold exists as multicellular filaments called hyphae.

They can be septate or aseptate (aka ceonocytic).

40
Q

What do fungi do when the environmental conditions suck?

A

They form spores (from meiosis or mitosis) or conidia (type of spore resulting from mitosis - asexual -that bud off of condidophore structures)

41
Q

Define definitive host, intermediate host, and carrier host.

A

Definitive hosts carry the adult or sexual stage of a parasite.

Intermediate hosts harbor a larval or asexual form of a parasite while the parasite is developing.

Carrier hosts harbor a larval or asexual form of a parasite while the parasite is not undergoing development.

42
Q

What is an inflammasome?

A

A cytosolic protein complex that helps amplify the inflammatory response after NOD-like receptors bind PAMPs.

43
Q

What types of things activate NOD-like receptors, leading to the formation of the inflammasome and activation of caspase-1?

A

K+ efflux from the cell (in response to bacterial infection), unmethylated CpG DNA, ssRNA, dsRNA, release of ROS from ruptured phagolysosomes, inflammatory cytokines, other DAMPs and PAMPs inside the cell.

44
Q

What are the two major steps for inflammasome formation?

A

Priming - translation of inflammasome components.

Activation by DAMPs, PAMPs, etc.

45
Q

How do bacteria get iron from their hosts?

A

They put out siderophore proteins that bind iron tightly, then use siderophore receptors to engulf the sideophore-iron complexes.

Some also have lactoferrin and transferrin receptors that are used to take in iron.

46
Q

Are microbes that live inside host cells safe from complement?

A

Yeah

47
Q

Where is TLR2 and what does it recognize?

A

Plasma membrane, recognizes peptidoglycan/lipotechoic acid

48
Q

Where is TLR4 and what does it recognize?

A

Plasma membrane, recognizes LPS.

49
Q

Where is TLR9 and what does it recognize?

A

Endosomal, recognizes unmethylated CpG DNA

50
Q

After NOD-like receptors are activated, they cleave pro-caspase 1 –> caspase 1, which then cleaves pro-forms of…?

A

IL-1

51
Q

What is the intracellular part of a TLR called?

A

TIR

52
Q

Which cytokines make endothelial cells sticky?

A

IL-1, TNF, C5a, leukotriene B

53
Q

Describe the signaling pathway that results in TNF-alpha production.

A

PAMP binds to PRR (like a TLR or something) and the adapter protein MyD88 goes and tells the NFkB transcription factor to upregulate transcription of TNF-alpha genes.

54
Q

Name a few cell types that make IL-6 and state what IL-6 does.

A

Macrophages, endothelial cells, fibroblasts make it. It stimulates liver synthesis of acute phase reactants and induces TH17 T cells to make IL-17 to activate neutrophils, and causes fever.

55
Q

When Type 1 interferons bind to innate resident cells, three big anti-viral changes occur. What are they?

A
  1. Inhibition of viral protein synthesis.
  2. Degradation of viral RNA.
  3. Inhibition of viral gene expression and virion assembly.
56
Q

Which chemokine is the major chemokine for neutrophil chemotaxis?

A

IL-8

57
Q

Which type of leukocyte is the major player during resolution of tissue injury? What do these cells do?

A

Macrophages eat up dead stuff and make proteases and growth factors that promote tissue repair.

58
Q

Describe how NK cells participate in antibody-dependent cellular cytotoxicity.

A

NK cells have IgG Fc receptors that bind the Fc portion of IgGs that have attached to infected cells –> kill with Perforin, Granzyme B, and Fas ligand

59
Q

What does histamine do to parasites? Which cells make histamine?

A

Histamine kills parasites, eosinophils and mast cells make histamine.

60
Q

What are the steps in leukocyte extravasation?

A
  1. Margination and rolling (selectins on endothelial cells bind loosely to selectin ligands on leukocytes)
  2. Integrin activation by chemokines puts integrins on leukocytes in a high affinity state
  3. Firm adhesion between integrins on leukocytes and CAMs on endothelial cells.
  4. Transmigration (CD31 mediated) to the site of the antigen in the tissue with chemokines like C5a, Leukotriene B, and IL-8.
61
Q

What is Leukocyte Adhesion Deficiency type 1 and what causes it?

What causes LAD-2?

A

LAD-1: CD-18 integrin mutation, AR inheritance. No firm binding for leukocyte extravasation. Delayed wound healing, umbilical cord takes a long time to fall off.

LAD-2: lack of enzyme that makes selectin ligands on leukocytes.

Both are characterized by recurrent bacterial and fungal infections.

62
Q

Describe the protein cascade involved in the classical complement pathway.

A

C1q binds to the Fc region of an IgG or IgM-antigen complex (immune complex) –> C1r –> C1s –> C4b –> C2a –> cuts C3 –> C3b binds –> cuts C5 –> C5b binds –> C6, 7, 8, 9 join to make the membrane attack complex.

q r s 4b 2a 3b 5b 6 7 8 9

63
Q

Which protein is the major opsonin of complement?

A

C3b

64
Q

Name three anaphylatoxins produced by the complement cascade. What are anaphylatoxins?

A

C3a, C4a, C5a

Anaphylatoxins can degranulate mast cells and basophils

65
Q

Name two chemokines that are produced by the complement cascade.

A

C3a, C5a

66
Q

Specifically what on a bacteria can activate the lectin complement pathway?

Describe the pathway.

A

Mannose sugars on bacteria.

Mannose-binding lectin (MBL) binds to mannose on bacteria –> MASP1 and MASP2 join –> C2 and C4 are cleaved –> C4bC2a cleaves C3 –> C3b binds –> C5 cleavage –> C5b, 6, 7, 8, 9 form the MAC

67
Q

How does the alternative complement pathway work?

A

C3 normally floats around in the blood and is naturally degraded into C3a and C3b. C3b binds to LPS on gram-negative bacteria and initiates the alternative pathway.

Factor B binds to C3b on the bacteria –> Factor D –> Properdin stabilizes

C3bBbP is the C3 convertase that splits C3 –> C3a and C3b and the pathway continues down to C9

68
Q

How do phagocytes recognize opsonins like C3b?

A

Phagocytes express complement receptor 3 on their surface that binds the C3b on bacteria, then they eat the bacteria.

69
Q

Which neutrophil precursor cell is the last one capable of mitosis?

A

Neutrophilic myelocytes

70
Q

What does a left shift in a peripheral blood smear mean? What might it indicate?

A

It means there are more precursor cells to neutrophils in the peripheral blood. Indicative of possible bacterial infection or leukemia.

71
Q

What is another term for attributable risk?

A

Risk difference

72
Q

What does PGI2 do?

A

Vasodilation, increased permeability

73
Q

What does PGE2 do?

A

Vasodilation, increased permeability, fever, pain

74
Q

What does PGD2 do?

A

Vasodilation, increased permeability

75
Q

What do LTC4, LTE4, and LTD4 do?

A

Vasoconstriction, increased permeability, bronchospasm

MS1 - Invaders and Defenders aka Clusterfuck (16 decks)

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