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Winter 2016 > B&L Unit 2 > Flashcards

B&L Unit 2 Flashcards

1
Q

What does IFN-y do?

A

Chemotactic for monocytes

Classically activates macrophages

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2
Q

2 things classically activates macrophages secrete

A

TNF-alpha

IL-1

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3
Q

What 2 lymphokines do Th1 cells secrete?

A

IFN-y - chemotactic, activates macrophages

IL-2 - activates killer T cells

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4
Q

What are 5 things the Th0 cell can differentiate into?

A 
TH1
THh17
Th2
Tfh
Treg
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5
Q

3 things that alternatively activate macrophages

A

IL-4
IL-5
IL-13

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6
Q

What do alternatively activated macrophages do? (4)

A

Healing stuff
Debris removal
Scar formation
Walling off pathogens

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7
Q

Which cell classically activates macrophages and which one alternatively activates macrophages

A

Th1

Th2

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8
Q

Where to Tfh cells hang out?

A

Lymph node follicles, where the B cells are

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9
Q

What do Tfh cells do?

A 
They help B cells that have recognized antigen activate and differentiate into plasma cells
Get them to do class switching as well
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10
Q

What do Tregs do?

A

Suppress activation and function of other Th cells

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11
Q

What 3 things do Tregs make?

A

Foxp3 transcription factor
TGFbeta
IL-10

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12
Q

What are the two ways a killer T cell can induce apoptosis in its target cell?

A

Engagement of death receptor Fas with Fas ligant

Secrete lytic granules that contain granzymes and perforins

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13
Q

What 2 things do killer T cells require for activation?

A

Contact with antigen-bearing dendritic cell

IL-2 from Th1 cells

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14
Q

Which CD is on the surface of basically all T cells?

A

CD3

It is part of the TCR

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15
Q

Which CD identifies B cells?

A

CD20

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16
Q

Which CD identifies helper T cells?

A

CD4

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17
Q

Which CD identifies killer T cells?

A

CD8

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18
Q

T cells are _________-specific and _________-restricted

A

Antigen

MHC (major histocompatibility complex)

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19
Q

Do T cells see free antigen?

A

No. They see antigen only when it is complexed with cell-surface MHC molecules

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20
Q

What are the 2 TCR (T cell receptor for antigen) chains?

A

Alpha

Beta

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21
Q

What does CD3 do for the T cell?

A

Transduces TCR signals

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22
Q

Where are MHC class I products locate? Class II?

A

MHCI is on all nucleated cells

MHCII is on dendritic and macrophage cells

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23
Q

What is the gene structure for the T-cell receptor alpha chain? Beta chain?

A

V and J
V, D, and J

A different gene than the B cell one!

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24
Q

Killer T cells look at antigens with MHC class______ molecules and Th cells look at antigens with MHC class _____ olecules

A

I - because they look for infected cells

II

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25
Q

What is cross-presentation?

A

Dendritic cells (ONLY dendritic cells) can present antigens to class I and class II MHC at the same time

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26
Q

What is a mitogen?

A

An agent that stimulates T cell mitosis

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27
Q

Ligands for the ___________ receptor are unique to the thymus and guide T cell precursors

A

Notch

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28
Q

What other 2 unique things do double-negative cells express?

A

Rag-1 and Rag-2 DNA recombinases

Help rearrange TCR V(D)J genes

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29
Q

When are T cell precursors double negative? When are they double positive?

A

When they first get to teh thymus

Before selection. They turn off one or the other during selection.

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30
Q

What does a T cell recognize?

A

Antigenic peptide + self MHC

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31
Q

T cells are positively selected for ___________ affinity and negatively selected for ___________ affinity

A

Self MHC

Self other things

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32
Q

How do T cells get selected against for other body stuff when in the thymus? How do they encounter it?

A

AIRE (autoimune regulator) gene causes thymic stromal/epithelial cells to express a wide variety of peptides expressed elsewhere in the body

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33
Q

What happens to non-selected T cells?

A

If they have no MHC affinity and no self (non MHC) affinity, they are not stimulated through their TCRs. Apoptosis in 2-3 days

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34
Q

Which HLA loci do we care about? Which is most important for transplants?

A

HLA-A
B
D

DR

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35
Q

HLA expression is ___________ (like recessive, dominant, etc)

A

Codominant

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36
Q

What is the structure of MHC class I and II

A

Glycoproteins composed of two poplypeptide chains

Class I has a variable chain with a constant beta2-microglobulin chain

Class II has 2 variable chains (alpha and beta)

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37
Q

Do minor histocompatibility antigens cause acute or chronic rejection?

A

Chronic

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38
Q

In graft rejection, Th1 cells recognize foreign ___________ on ___________ and ___________ cells
Killer T cells recognize ___________ and ___________ on ___________ cells

A

HLA-DR
Macrophages from graft
Dendritic cells from graft

HLA-A
HLA-B
All graft cells

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39
Q

People with ankylosing spondylitis often are HLA___________

A

B27

40
Q

Why do blood vessels bypass the cortex in the thymus?

A

Ensures differentiating T cells don’t get exposed to blood antigens until they are fully differentiated

41
Q

At what age does thymus involution begin?

A

Onset of puberty

42
Q

Where are B cells in the lymph node? Where are T cells?

A

Cortex

Paracortex

43
Q

Where do lymphocytes enter the lymph nodes? What is special about these tissues?

A

Postcapillary venules

High, cuboidal endothelial cells

44
Q

What are Hassal’s corpuscles made of? Where are they?

A

Concentric layers of reticular cells

In thymus medulla

45
Q

What is special about splenic blood flow?

A

Discontinuous endothelium so that an open circulation occurs

46
Q

Where is most of the lyphoid tissue in the spleen?

A

Periarteriolar lymphoid sheath

47
Q

Where are germinal centers in the spleen?

A

Periarteriolar lymphoid sheath

48
Q

Lymphokines are a subfamily of ___________

A

cytokines

49
Q

What 2 factors classically activate macrophages?

A

IFN-Y

IL-1

50
Q

What 2 things does IL-4 do?

A

Alternatively activate macophages

Chemotactic for eosinophils

51
Q

What is the extrinsic pathway (of idk T cell something)

A

APCs take in antigen, digest it, and put it on MCH class II

52
Q

What is immune surveillance?

A

Body cells put things from inside them on their surface MHC receptors so that the immune system can decide if they are normal or not.
This makes sure body cells aren’t making foreign or mutated proteins

53
Q

What is antien cross-presentation?

A

An APC puts antigen on class I and class II MHC

When Th1 looks at the antigen on class II, it makes IGN-Y and IL-2
IL-2 and the antigen on MHC I activates the killer T and then it goes around fucking shit up on other cells displaing this antigen
54
Q

What is T-independent B cell activation?

A

For antigens whose epitopes are regular and joined, usually carbohydrates

This alone gives the B cell enough signal that it gets activated and makes antibody

It does not class switch, however

55
Q

What is a cytokine storm? What causes it?

A

Lectins can stick to sugars on T cell receptors, fooling the T cell into thinking its binding antigen and activating

Mitogen! This stimulates all the T cells to get activated at the same time and make lots of cytokines

56
Q

What are the fates of a pre-T cell?

A

No CDR binding -> no signal -> it dies because it doesn’t recognize the MHC

Complete CDR binding -> it is autoimmune -> dies or becomes a Treg

57
Q

4 important environmental toxins

A

Polycyclic aromatic hydrocarbons
Aromatic amines
Nitrosamines
Aflatoxin

58
Q

What is the MHC gene organization?

A

ClassII: DP/DQ/DR
Class III: C4/Bf/C2/TNF
Class I: B/C/A

Chromosome 6

59
Q

Do HLA genes experience recombination?

A

No. Linkage disequilibrium occurs.

60
Q

How does a mixed leukocyte reaction work?

A

Get blood monocytes from the donor by irradiating blood (kills lymphocytes)

Check if Th cells from the recipient recognize the monocytes form the donor

61
Q

What is the Ames test? What information does it provide?

A

A screen to decide which chemicals should be tested for carcinogenic potential in animals.

Take Salonella typhimurium that are His- (require histidine). Put them in media w/o histidine and liver microsomal enzymes. If the chemical is mutagenic then His+ mutants will form

62
Q

What are the 2 stages of cancer development with carcinogens?

A
  1. Initiation. Direct effect of a carcinogen and is irreversible.
  2. Promotion. Effect of a noncarcinogen. Is reversible and requires repeated application after initiation
63
Q

Why does inflammation promote cancer? 2 reasons

A

Production of oxygen radicals are
Mutagenic
Promote cell proliferation

64
Q

What does tumor invasion mean (of an epithelial cancer)?

A

Tumor cells have broken through the basement membrane that separates the epithelium from connective tissue stroma

65
Q

What is a conjugate vaccine?

A

Antigen that is coupled to a protein ‘carrier’ to which Tfh cells can respond
This increases B cell activation in response to the antigen

66
Q

What are vaccine adjuvants?

A

Substances added to vaccines to make them more immunogenic

They produce an innate immune response, leading to a better adaptive response

67
Q

What 2 things cause cavities?

A
  1. Bacteria and stuff

2. Immune response

68
Q

How long does it take to make a neutrophil under regular conditions? What about stressed conditions?

How long does it stay in the blood?

A

10-14 days
5 days

6 hours

69
Q

How many neutrophils does a neutropenic adult have?

A
70
Q

How many neutrophils does an adult have who has neutrophilia?

A

> 7500 / uL

71
Q

How long does the monocyte stay in the marrow? The intravascular compartments? Tissues?

A

7 days
3-5 days
days-months

72
Q

What does the monocyte nucleus look like?

A

Kidney-shaped

73
Q

Which cytokine induces eosinophil production?

A

IL-5

74
Q

What does the eosinophil nucleus look like?

A

Bi-lobed

75
Q

What are the 5 mechanisms by which infection-associated neutropenia can occur?

A
  1. Increased utilization
  2. Complement-mediated margination
  3. Marrow suppression/failure
  4. Cytokine/chemokine induced margination
  5. Anti-neutrophil antibody production
76
Q

What is left shift of a differential?

A

Increase in neutrophils (segs and bands) on the differential

77
Q

3 cells that aren’t B cells in the germinal center

A

Tingible body macrophages
follicular dendritic cell
T helper cells

78
Q

Whee do macrophages hang out in lymph nodes?

A

In the subcapular space

79
Q

What is a syngenic graft/isograft?

A

A transplant between identical twins

80
Q

What are the ‘arms’ of the phagocyte in opsonization?

A

Pseudopods

81
Q

What are the 4 main reactive oxygen species?

A

Superoxide O2*
Hydrogen peroxide H2O2*
Hypochlorous acid HClO*
Hydroxyl radical *OH

82
Q

What is the molecular defect and inheritance pattern of leukocyte adhesion deficiency I?

A

CD18 -> lack of expression of CD11b/CD18

Autosomal recessive

83
Q

What is the functional defect in leukocyte adhesion deficiency I?

A

Neutrophilia (so like more in the blood)

Decreased adherence to the endothelial surface, so the neutrophils can’t get to where they need to go

84
Q

What 3 things happen clinically in leukocyte adhesion deficiency I?

A

Recurrent soft tissue infections
Delayed separation of umbilical cord
Poor wound healing

85
Q

What is the molecular defect and inheritance pattern of chronic granulomatous disease?

A

Defects in one of the 4 oxidase components

Recessive (autosomal or X-linked)

86
Q

What is the functional defect in chronic granulomatous disease?

A

Neutrophila, but they can get to where they need to go just fine
Defect in the oxidase enzyme system

87
Q

What is the molecular defect and inheritance pattern of Chediak-Higashi syndrome?

A

Alterations in membrane fusion -> giant, leaky granules
Problems w/ utubule assebly

Autosomal recessive

88
Q

What is the functional defect in Chediak-Higashi syndrome?

A

Neutropenia
Giant granules in all luekocytes
Abnormal degranulation
Decreased degranulation, microbicidal activity
Movement defects (of muscles or intercellularly?

89
Q

What 3 things happen clinically in Chediak-Higashi syndrome?

A 
Albinism
Nystagmus photophobia
Recurrent infections by bacteria
Lymphoproliferative disease with stuff
Neurodegenerative syndrome
90
Q

What is the molecular defect and inheritance pattern of myeloperoxidase deficiency?

A

Post-translational modification defect in processing the protein
Autosomal recessive

91
Q

What is the functional defect in myeloperoxidase deficiency?

A

Partial or complete loss of myeloperoxidase
Mid defect in killing bacteria
Significant defect in killing candida

92
Q

What 1 thing happens clnically in myeloperoxidase deficiency?

A

Increased fungal infections when diabetes present

93
Q

What happens in C3 (complement) deficiency?

A

Inefficient opsonization of bacteria -> recurrent bacterial infections

94
Q

What happens in C5-C9 deficiencies?

A

Increased risk for Neisseria bacterial infections

95
Q

What happens in 1q, C4, and C2 deficiencies?

A

Increased risk of systemic lupus or other autoimmue/inflammatory vascular diseases

96
Q

What compound results in neutrophil proliferation?

A

G-CSF

97
Q

What infections are more common with chronic granulomatous disease?

A

Catalase-positive organisms

Winter 2016 (8 decks)

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