Lecture #1 -- Innate and Adaptive Immunity Flashcards

1
Q

Name some phagocytes.

A

Macrophages (Tissue Residents)
Neutrophils (Recruited from Blood)
Dendritic Cells (Tissue Residents)

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2
Q

What types of immune cells do peptides turn on?

A

ab-T cells and B cells

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3
Q

What types of immune cells do glycoproteins/carbohydrates turn on?

A

B cells, Macrophages/Neutrophils/DCs/Tissue Cells

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4
Q

What types of immune cells do glycolipids and phospholipids turn on?

A

B cells

NKT cells, gd-T cells

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5
Q

What types of immune cells do peptidoglycans/nucleic acids/flagella turn on?

A

B cells

Mac/Neu/DC/Tissue via TLRs

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6
Q

Name phagocyte cell surface receptors

A

Complement, Fc, MHC Class II, TLR

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7
Q

Name some chemotactic agents.

A

C5a, LTB4, Chemokines (IL-8, MIP, MCP)

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8
Q

Name some ways phagocytes can kill bacteria.

A

Metabolic Burst
Superoxide (via NADPH oxidase)
H2O2 (via Superoxide Dismutase)
Acid Hydrolases, Muramidase, Lysozyme, Defensins

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9
Q

Name the two types of receptors on a macrophage.

A

Phagocytic receptor and signaling receptor

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10
Q

Cytokines involved in inflammation?

A

Il-1, TNF-a, IL-6, CXCL8, IL-12

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11
Q

What does IL-1/TNF-a do?

A

Increase BV permeability

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12
Q

What does IL-6 do?

A

Increase fat/muscle metabolism –> Fever

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13
Q

What does CXCL8 do?

A

Recruits neutrophils

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14
Q

What does IL-12 do?

A

Recruits/Activates NKs, strengthen Mac response

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15
Q

What cytokine induces acute phase proteins? Where are they made? Name three.

A

IL-6
Liver
CRP, Fibrinogen, Mannose-binding Protein

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16
Q

What do acute phase proteins do?

A

Opsonization and Complement Activation

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17
Q

What is sepsis?

A

Systemic Inflammatory response due to Infection

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18
Q

What two parts does C3 split into? What do they do?

A

C3a – Recruits Phagocytes

C3b – Tags bacterium for destruction

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19
Q

How does C3b affect bacterium after binding?

A

Binds macrophage CR1, causing endocytosis

After endocytosis, eventually phagolysosome breaks up bac.

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20
Q

Receptors on Macrophages?

A

Complement receptor 3/4 (Mac-1)
LPS Receptor (CD14)
Toll Like Receptors

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21
Q

What are the components involved in LPS recognition?

A

CD14, TLR4, MD2, LPS

X2 (its a dimer)

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22
Q

What does TLR 2/6 recognize? Where is it located?

A

Lipoteichoic Acid/Zymosin

Plasma Membrane

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23
Q

What do TLR 4/4 homodimers recognize? Where are they located?

A

LPS

Plasma Membrane

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24
Q

What does TLR9 recognize? Where is it located?

A

Unmethylated CpG-rich DNA

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25
Q

Describe the molecular steps of TLR activation.

A

TLR–>TIR Domain–>MyD88–>IRAK4–>TRAF6–>IKK–>Degradation of IkB –> NFkB transcribes cytokines

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26
Q

What receptor is unique to neutrophils?

A

N-formyl methionine receptor

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27
Q

What are competitors used in bacterial destruction?

A

Lactoferrin and B-12 binding protein

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28
Q

How do defensins work? What makes defensins?

A

electrically attracted to lipid bilayer, make pores. Made by paneth cells.

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29
Q

What are the steps of Leukocyte adhesion?

A

Rolling Adhesion, Tight Binding, Diapedesis, Migration

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30
Q

What molecule facilitates rolling adhesion?

A

Selectins

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31
Q

What molecule facilitates tight binding?

A

Chemokines (like CXCL8)

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32
Q

What molecule facilitates diapedesis?

A

Integrins (like ICAM-1)

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33
Q

What molecule facilitates migration?

A

Chemokines

34
Q

ID markers on NK cells?

A

CD14 and CD 56

35
Q

What do NK cells secrete?

A

IFN-g, IL-1, CM-CSF, TNF-a

36
Q

How do NK cells work in immune response?

A

Use perforin on MHC fuck ups or promote Ab-dependant cytotoxicity

37
Q

Activating receptors for NK cells?

A

MIC-A,B, Fc

38
Q

Inhibitory receptors for NK cells?

A

HLA Class I, HLA B,C

39
Q

What cytokines turn on NK response?

A

IFNa, IFNb, TNFa, IL-12

40
Q

What do interferons do?

A

Interfere with viral infection

  • Induce resistance to viral replication
  • Increase NK ligand expression and Activation
41
Q

What happens in Antibody Dependant Cell-Mediated Cytotoxicity?

A

Fc receptors on NK cells recognize bound Ab, trigger kill response

42
Q

What type of Ab do Fc’s usually respond to?

A

IgG

43
Q

Who has FcR 1? CD#?

A

Macrophages, Monocytes

64

44
Q

Who has FcR 2? CD#?

A

B cells, Neutrophils, Macrophages, Monocytes

32

45
Q

Who has FcR 3? CD#?

A

NK cells, Neutrophils, Macrophages

16

46
Q

How are Mast cells activated?

A

Ig-E binds FcR 1

47
Q

What five tasks are Fc Receptors important for?

A
Phagocytosis and Killing (FcRIII for NK, I/II for Phago)
Mediator Release (FcRI on Mast Cells)
Enhancement of Uptake
B-cell negative feedback
Complement Activation
48
Q

Give examples of primary and secondary lymphoid tissues.

A

Primary – Bone Marrow/Fetal Liver, Thymus

Secondary – Lymph Nodes, Spleen, MALT

49
Q

Describe a lymphoid cell working around the system starting in high endothelial venules.

A

High Endothelial venules –> efferent lymphatic vessels –> thoracic duct -> blood lymphocyte pool –> afferent lymphatic vessels

50
Q

Where do CD3+ T cells become functional?

A

LN Cortex/Paracortex

51
Q

Where do CD19+ B cells differentiate?

A

Germinal Centers

52
Q

What are the roles of the white and red pulp of the spleen?

A

WP – Lymph Node

RP – Blood Filter

53
Q

Name the lymphocytes.

A

B cell, T Cell, NK Cell

54
Q

Name Antigen Presenting Cells

A

DC, Macrophage, B Cell

55
Q

Name Effector Cells

A

T Cell, Macrophage, Granulocytes

56
Q

How much faster is secondary immune response?

A

1.5-2 weeks

57
Q

Role of CD4 T Cells?

A

Control of B cells and macrophages

58
Q

Mechanical antimicrobial factors.

A

Mechanical barrier of skin
Mucous epithelial barrier
Ciliated epithelium
Normal Microflora

59
Q

Name the innate immunity cells

A
Neutrophils
Macrophages
NK
Mast Cells
Eosinophils, Basophils
Dendritic Cells
60
Q

Name oxygen dependent antibacterial factors.

A

Superoxide (from NADPH oxidase)
Hydrogen Peroxide (Superoxide dismutase)
Hypochlorite (myeloperoxidase)

61
Q

Name oxygen independent antimicrobials

A
Acid hydrolases
Muramidase
Lysozyme
Lactoferrin
Defensins
62
Q

Major cytokines of Sepsis?

A

TNF-alpha, IL-1, IL-6

63
Q

Two macrophage receptors that recognize microbial products.

A

TLR, LPS receptor

64
Q

Two macrophage receptors that bind pathogens

A

Mannose Receptor
CR3
Glucan Receptor
Scavenger Receptor

65
Q

When do you see neutrophils in tissue?

A

Only in infection/inflammation

66
Q

Macrophage receptors used for identification in phagocytosis?

A

CTLD
Dectin-1
Complement Receptors
SR-A, SR-B

67
Q

Basic methods used by phagolysosomes (6)

A
Acidification
Toxic Oxygen
Toxic NO
Antimicrobial Peptides
Enzymes
Competitiors
68
Q

How do defensins work?

A

Electrostatic attraction brings them to lipid bilayer
Defensins bind together to form pores
Loss of osmotic control = dead bacteria

69
Q

T of F. Many neutrophils must be generated at the onset of an infection.

A

F. Large neut. reserves are stored in the marrow for rainy days

70
Q

What happens to neutrophils in battle?

A

They engulf and kill bacteria
Die nobly in the tissue
Engulfed and degraded by macrophages

71
Q

What percentage of circulating lymphocytes are NKs?

A

10-15%

72
Q

What is the murder weapon of choice for NK cells?

A

Perforin

73
Q

Significance of NKs in cancer?

A

NK cells attack tumor cells lacking MHC I

74
Q

Significance of inhibitory and activating receptor activity in NK cell.

A

Inhib binds MHC Class 1
Activating binds activating ligands

Activation + No Inhib = Targeted Killing
Activation + Inhib = Depends on balance of signals

75
Q

Receptor utilized in Antibody-dependent-cell-mediated toxicity?

A

CD16/Fc-gamma-RIII

76
Q

Difference in T/B Cell Life cycle compared to neutrophil.

A

T/B can beome memory cells, be recycled through circulation many times.

Neutrophils are on a one way trip

77
Q

Name the gut-associated lymphoid tissue.

A

Peyer’s Patches

78
Q

Of the APCs, which is prone to prsent to T cells? B cells?

A

Dendritic Cells. Follicular Dendritic Cells.

79
Q

Microbial primary target for B cell, CD4 helper, CD8 cytotoxic

A

B – Extracellular Microbes
CD4 – Phagocytosed Microbes
CD8 – Intracellular Microbes (like viruses)

80
Q

Difference in peptide bonding of Antibody and TCRs?

A

Antibody recognizes whole proteins

TCRs recognize small peptide pieces presented by dendritics

81
Q

Phases of a T cell response

A

Clonal Expansion
Differentiation
Cell Mediated Immunity
Apoptosis/Survival as Memory Cells