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Lecture #1 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 cellsNKT cells, gd-T cells

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5
Q

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

A

B cellsMac/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 BurstSuperoxide (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-6LiverCRP, 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 PhagocytesC3b – Tags bacterium for destruction

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19
Q

How does C3b affect bacterium after binding?

A

Binds macrophage CR1, causing endocytosisAfter 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, LPSX2 (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

LPSPlasma 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
Describe the molecular steps of TLR activation.
TLR-->TIR Domain-->MyD88-->IRAK4-->TRAF6-->IKK-->Degradation of IkB --> NFkB transcribes cytokines
26
What receptor is unique to neutrophils?
N-formyl methionine receptor
27
What are competitors used in bacterial destruction?
Lactoferrin and B-12 binding protein
28
How do defensins work? What makes defensins?
electrically attracted to lipid bilayer, make pores. Made by paneth cells.
29
What are the steps of Leukocyte adhesion?
Rolling Adhesion, Tight Binding, Diapedesis, Migration
30
What molecule facilitates rolling adhesion?
Selectins
31
What molecule facilitates tight binding?
Chemokines (like CXCL8)
32
What molecule facilitates diapedesis?
Integrins (like ICAM-1)
33
What molecule facilitates migration?
Chemokines
34
ID markers on NK cells?
CD14 and CD 56
35
What do NK cells secrete?
IFN-g, IL-1, CM-CSF, TNF-a
36
How do NK cells work in immune response?
Use perforin on MHC fuck ups or promote Ab-dependant cytotoxicity
37
Activating receptors for NK cells?
MIC-A,B, Fc
38
Inhibitory receptors for NK cells?
HLA Class I, HLA B,C
39
What cytokines turn on NK response?
IFNa, IFNb, TNFa, IL-12
40
What do interferons do?
Interfere with viral infection - Induce resistance to viral replication- Increase NK ligand expression and Activation
41
What happens in Antibody Dependant Cell-Mediated Cytotoxicity?
Fc receptors on NK cells recognize bound Ab, trigger kill response
42
What type of Ab do Fc's usually respond to?
IgG
43
Who has FcR 1? CD#?
Macrophages, Monocytes64
44
Who has FcR 2? CD#?
B cells, Neutrophils, Macrophages, Monocytes32
45
Who has FcR 3? CD#?
NK cells, Neutrophils, Macrophages16
46
How are Mast cells activated?
Ig-E binds FcR 1
47
What five tasks are Fc Receptors important for?
Phagocytosis and Killing (FcRIII for NK, I/II for Phago)Mediator Release (FcRI on Mast Cells)Enhancement of UptakeB-cell negative feedbackComplement Activation
48
Give examples of primary and secondary lymphoid tissues.
Primary -- Bone Marrow/Fetal Liver, ThymusSecondary -- Lymph Nodes, Spleen, MALT
49
Describe a lymphoid cell working around the system starting in high endothelial venules.
High Endothelial venules --> efferent lymphatic vessels --> thoracic duct -> blood lymphocyte pool --> afferent lymphatic vessels
50
Where do CD3+ T cells become functional?
LN Cortex/Paracortex
51
Where do CD19+ B cells differentiate?
Germinal Centers
52
What are the roles of the white and red pulp of the spleen?
WP -- Lymph NodeRP -- Blood Filter
53
Name the lymphocytes.
B cell, T Cell, NK Cell
54
Name Antigen Presenting Cells
DC, Macrophage, B Cell
55
Name Effector Cells
T Cell, Macrophage, Granulocytes
56
How much faster is secondary immune response?
1.5-2 weeks
57
Role of CD4 T Cells?
Control of B cells and macrophages
58
Mechanical antimicrobial factors.
Mechanical barrier of skinMucous epithelial barrierCiliated epitheliumNormal Microflora
59
Name the innate immunity cells
NeutrophilsMacrophagesNKMast CellsEosinophils, BasophilsDendritic Cells
60
Name oxygen dependent antibacterial factors.
Superoxide (from NADPH oxidase)Hydrogen Peroxide (Superoxide dismutase)Hypochlorite (myeloperoxidase)
61
Name oxygen independent antimicrobials
Acid hydrolasesMuramidaseLysozymeLactoferrinDefensins
62
Major cytokines of Sepsis?
TNF-alpha, IL-1, IL-6
63
Two macrophage receptors that recognize microbial products.
TLR, LPS receptor
64
Two macrophage receptors that bind pathogens
Mannose ReceptorCR3Glucan ReceptorScavenger Receptor
65
When do you see neutrophils in tissue?
Only in infection/inflammation
66
Macrophage receptors used for identification in phagocytosis?
CTLDDectin-1Complement ReceptorsSR-A, SR-B
67
Basic methods used by phagolysosomes (6)
AcidificationToxic OxygenToxic NOAntimicrobial PeptidesEnzymesCompetitiors
68
How do defensins work?
Electrostatic attraction brings them to lipid bilayerDefensins bind together to form poresLoss of osmotic control = dead bacteria
69
T of F. Many neutrophils must be generated at the onset of an infection.
F. Large neut. reserves are stored in the marrow for rainy days
70
What happens to neutrophils in battle?
They engulf and kill bacteriaDie nobly in the tissueEngulfed and degraded by macrophages
71
What percentage of circulating lymphocytes are NKs?
10-15%
72
What is the murder weapon of choice for NK cells?
Perforin
73
Significance of NKs in cancer?
NK cells attack tumor cells lacking MHC I
74
Significance of inhibitory and activating receptor activity in NK cell.
Inhib binds MHC Class 1Activating binds activating ligandsActivation + No Inhib = Targeted KillingActivation + Inhib = Depends on balance of signals
75
Receptor utilized in Antibody-dependent-cell-mediated toxicity?
CD16/Fc-gamma-RIII
76
Difference in T/B Cell Life cycle compared to neutrophil.
T/B can beome memory cells, be recycled through circulation many times. Neutrophils are on a one way trip
77
Name the gut-associated lymphoid tissue.
Peyer's Patches
78
Of the APCs, which is prone to prsent to T cells? B cells?
Dendritic Cells. Follicular Dendritic Cells.
79
Microbial primary target for B cell, CD4 helper, CD8 cytotoxic
B -- Extracellular MicrobesCD4 -- Phagocytosed MicrobesCD8 -- Intracellular Microbes (like viruses)
80
Difference in peptide bonding of Antibody and TCRs?
Antibody recognizes whole proteinsTCRs recognize small peptide pieces presented by dendritics
81
Phases of a T cell response
Clonal ExpansionDifferentiationCell Mediated ImmunityApoptosis/Survival as Memory Cells

Immunology (10 decks)

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