Immunology Flashcards

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1
Q

What is the difference between first-degree and second-degree immune organs?

A

First-degree: where immune cells develop (i.e., bone marrow and the thymus)
Second-degree: where immune cells are assisted (spleen, lymph nodes, tonsils, Peyer patches)

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2
Q

True or false: lymph nodes typically have more afferent vessels than efferent vessels.

A

True.

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3
Q

What is the main role of the lymph node medulla?

A

To communicate with the efferent lymphatic; medullae are typically T cells, B cells, and macrophages

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4
Q

Which part of the lymph node is likely to be impaired or underdeveloped in children with DiGeorge?

A

The paracortex

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5
Q

The superficial inguinal lymph nodes drain everything below the umbilicus with a few exceptions: ________________.

A

the testes, ovaries, and uterus drain into the para-aortic lymph nodes; the posterior calf and dorsolateral foot drain into the popliteal lymph nodes

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6
Q

T cells and B cells reside in which parts of the spleen?

A

T cells: periarteriolar lymphatic sheath

B cells: germinal centers

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7
Q

Where do macrophages catch encapsulated bacteria in the spleen?

A

In the marginal zone between the red pulp (RBCs) and white pulp (T cells and B cells, depending on the kind of white pulp)

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8
Q

What mechanism leads to immune vulnerability in post-splenectomy patients?

A

Decreased production of IgM –from decreased germinal centers –results in decreased complement activation, and complement activation is needed to kill encapsulated organisms.

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9
Q

What labs and histologic exams might you see in someone without a spleen?

A

Target RBCs
Lymph- and thrombocytosis (because they are normally sequestered in the spleen in a healthy person)
Howell-Jolly bodies (bits of DNA in RBCs normally removed by macrophages in the spleen)

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10
Q

Thymomas are associated with what two disorders?

A

Myasthenia gravis (no idea why) and superior vena cava syndrome

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11
Q

C-reactive protein is produced in response to _________. What does it do?

A

IL-6; it binds to dying cells –both human and bacterial – and stimulates the complement cascade to help get rid of cellular debris

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12
Q

One more time: which is MHC II, HLA-B or HLA-DR?

A

HLA-DR (“Two letters”)

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13
Q

True or false: MHC I is present on all cells.

A

False. It is not present on RBCs.

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14
Q

Which HLA types are associated with lupus?

A

D2 and D3 (“2 and 3 for S-L-E”)

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15
Q

Describe the maturation of T cells.

A

1) Bone marrow
2) Thymus cortex; CD4 and CD8 positive (positive selection: making sure it fits MHC)
3) Thymus medulla; CD4 or CD8 positive (negative selection: making sure it doesn’t recognize self-antigen)
4) Lymph node paracortex

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16
Q

Tonic expression of ___________ near M cells allows for development of Treg. Addition of __________ stimulates development of Th17.

A

TGF-beta; IL-6

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17
Q

IL-_____ down regulates Th1.

A

10 (produced by Treg)

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18
Q

Expression of the ________ gene is crucial during negative selection.

A

AIRE (because this causes thymic expression of proteins found throughout the body, thus ensuring that developing T cells can see all of the self-antigens)

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19
Q

Which interleukin stimulates development of Th2?

A

IL-4

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20
Q

Again, which interleukin stimulates Th1?

A

IL-12 (“twelve men to convict one prisoner”)

IL-12 is released by macrophages.

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21
Q

Describe the positive feedback between T cells and macrophages.

A

Macrophages secrete IL-12 which activates Th1 cells, and then Th1 cells secrete IFN-gamma which activates macrophages.

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22
Q

______________ kill cells with perforins and granzymes.

A

CD8+ T cells and NK cells

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23
Q

Which receptors do Tregs possess?

A

CD3, CD4, CD25, and FOXP3

(You already know the first two because they’re helper T cells, and you can use these mnemonics to recall the last two: 2x5 = 10, and Tregs secrete IL-10; and you need to be “cool as a fox” to help calm down your immune response.)

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24
Q

Diabetes in a male infant accompanied with dermatitis might be signs of _______________.

A

IPEX
Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked

A defect in the FOXP3 receptor that would normally allow Tregs to calm the body down.

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25
Q

The heavy chain contributes to ______________ and the light chain contribures to _______________.

A

the Fc and Fab regions; the Fab region

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26
Q

Why should you remember the Cs when it comes to the Fc region?

A

Complement binding
Constant
Carbohydrate side chain
Carboxy terminus

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27
Q

True or false: naive B cells express only IgD.

A

False. They express both IgM and IgD.

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28
Q

The complement-fixing antibodies include _______.

A

IgG and IgM

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29
Q

IgA circulates as __________.

A

monomers; it gets dimerized during transcytosis

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30
Q

Antigens lacking ___________ cannot be presented on MHC.

A

peptide exterior (that is, if they only have lipopolysaccharide such as Gram-negative bacteria, then APCs cannot present that in MHC)

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31
Q

What two receptor interactions are needed for T-cell activation?

A

MHC-II + antigen – CD4

CD80/86 (aka B7) – CD28

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32
Q

What two receptor interactions are needed for B-cell activation?

A

MHC-II + antigen –CD4

CD40 –CD40L

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33
Q

Five lab values with increase in response to acute inflammation and two will decrease. List them.

A

Increase:

  • CRP
  • Fibrinogen
  • Ferritin
  • Hepcidin
  • Serum amyloid A

Decrease:

  • Albumin
  • Transferrin
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34
Q

Which complement cytokines can cause anaphylaxis?

A

C3a, C4a, and C5a

AAA can cause anaphylaxis.

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35
Q

What proteins form the membrane attack complex?

A

C5b –C9b

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36
Q

Which complement protein attracts neutrophils?

A

C5b

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37
Q

What is the alternative complement pathway?

A

C3 can spontaneously lyse on bacterial surfaces (that is, without mannose-binding lectin or C1)

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38
Q

Trace the classical complement pathway.

A

Antigen-antibody complexes activate C1.

C1 cleaves C2 and C4.

C4b2b (aka C3 convertase) cleaves C3.

C4b2b3b (aka C5 convertase) cleaves C5, activating the MAC.

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39
Q

How is the alternative pathway different?

A

C3bBb acts as C3 convertase, and C3bBb3b –yes, two 3bs –acts as C5 convertase.

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40
Q

ACE inhibitors are contraindicated in those with what complement disorder?

A

C1 esterase deficiency (characterized by angioedema of the face)

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41
Q

GPI anchors what receptor?

A

Decay-accelerating factor, also called CD55

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42
Q

Again, what is the “Hot T Bone stEAK” mnemonic?

A
IL-1: fever
IL-2: T cell proliferation 
IL-3: bone marrow stimulant
IL-4: igE production
IL-5: igA production 
IL-6: aKute phase proteins (stimulating CRP)
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43
Q

In addition to causing fever, what does IL-1 do?

A

It promotes expression of adhesion molecules.

44
Q

IL-12 stimulates Th1 cells and __________.

A

NK cells

Going off your jury mnemonic for IL-12, think of TWELVE jurors sentencing ONE man because he’s a NATURAL-born KILLER.

45
Q

What does TNF-alpha do?

A

It causes vascular leaking, WBC recruitment, granuloma formation, and cachexia.

(“Trickling Nodular Fatigue Attractor”)

46
Q

Interferon-gamma inhibits the production of which lymphocyte?

A

Th2 cells (because interferon-gamma is secreted by Th1 cells)

47
Q

Which T cell type secretes IL-4, IL-5, and IL-10?

A

Th2

It secretes these to aid in granuloma formation and tamping down of the immune response.

48
Q

What pathway is inhibited in the X-linked immune disorder that presents with a negative methylene blue test?

A

O2 -> O2–• (NADPH oxidase)
O2–• -> H2O2 (superoxide dismutase)
H2O2 -> HCLO• (myeloperoxidase)

49
Q

Interferon alpha and beta primarily work to ______________.

A

prime uninfected cells to avoid spreading infection by down-regulating protein production

50
Q

Which receptor is specific to Treg?

A

CD25 (“25 regulations are too many”)

51
Q

All antigen-presenting cells have what two receptors?

A

MHC II and B7 (aka CD80/86)

52
Q

What receptor is specific to hematopoietic stem cells?

A

CD34

53
Q

True or false: T cells are not needed to activate macrophages.

A

True. When macrophages bind a PAMP – such as through their receptor CD14 –they become activated without any other signals.

54
Q

What does the “attenuated” part of live attenuated virus mean?

A

That the toxicity has been removed.

55
Q

Which vaccines are inactivated?

A

Rabies
Influenza (injection)
Polio (Salk)
Hepatitis A

(“RIP Always”)

56
Q

Explain the immune response that usually occurs with live and inactivated vaccines.

A

Live: cellular and humoral
Inactivated: humoral

57
Q

Describe the cellular mechanism behind type I hypersensitivity reactions.

A

IgE on mast cells and basophils bind and cross link antigen. This activates these cells and causes them to release histamine. Delayed inflammation arises from production of leukotrienes.

58
Q

Why do immune complexes cause damage?

A

They activate complement which attracts neutrophils (C5a). Neutrophils release cytotoxic enzymes.

59
Q

What is the Arthus reaction?

A

Injecting antigen into someone who has already developed antibody to that antigen leads a local immune complex lump that can lead to necrosis.

60
Q

There are two kinds of type IV hypersensitivity reactions: __________________.

A

CD8-mediated (in which T cells do the killing) and CD4-mediated (in which T cells activate macrophages that do the killing)

61
Q

What is a common cause of hyperacute anaphylaxis to blood transfusions?

A

Giving IgA-containing blood to individuals who are deficient in IgA

Note: this is a type I hypersensitivity reaction.

62
Q

True or false: hyperacute blood reactions are antibody-mediated.

A

False. Hyperacute reactions (those within minutes) are IgE-mediated and thus considered type I reactions. Antibody-mediated blood reactions present 1-6 hours after transfusion.

63
Q

There can be two kinds of type II hypersensitivity reactions to blood products: ________________.

A

hemolytic (in which antibodies are directed against RBCs) and nonhemolytic (in which antibodies are directed against WBCs)

64
Q

What causes acute lung reactions to blood products?

A

Donor anti-WBC antibodies attack in the lungs or attack pulmonary endothelium, leading to ARDS

65
Q

What antibody is commonly seen in type 1 diabetics?

A

Anti-glutamic acid decarboxylase

66
Q

Drug-induced lupus presents with anti-___________ antibodies.

A

histone

67
Q

Antibodies are needed to eliminate what virus?

A

Enterovirus and polio virus (hence, boys with Bruton’s will get polio if given live, Sabin polio vaccines)

68
Q

Which immune deficiencies are associated with autoimmune disease?

A

IgA deficiency and Wiskott-Aldrich syndrome

69
Q

_______________ is a defect in B-cell differentiation.

A

CVID (hence the normal levels of B cells and T cells and defective Ig/plasma cells)

70
Q

Which immune deficiency disorder presents with Th1 malfunctions?

A

Selective IL-12 receptor mutations

71
Q

What causes chronic mucocutaneous Candidiasis?

A

Selective defects in response to Candida antigens; otherwise normal

72
Q

What genetic inheritance pattern does the most common SCID disorder have?

A

XLR (being IL-2 receptor mutations)

Note: ADA deficiency is AR.

73
Q

Those with SCID will have decreased levels of __________.

A

serum TRECs

74
Q

The neurocutaneous disorder that presents with selective immunodeficiency has low levels of ______________.

A

IgA, IgG, and IgE

The run-in describes ataxia-telangiectasia which is caused by defects in DNA rearrangement.

75
Q

Those with CD-40L deficiency have high levels of ________ and are at increased risk of _______________.

A

IgM; pneumonia, Cryptosporidium, and CMV

76
Q

What causes Wiskott-Aldrich syndrome?

A

Defects in actin skeletons that prevent leukocyte cytoskeletal rearrangement and cause failure to show MHC

Remember: WA is XLR

77
Q

When would you worry about delayed umbilical cord?

A

Typically 30 days

78
Q

Which immune deficiency syndrome presents with enlarged granules in the cytosol?

A

Chédiak-Higashi

79
Q

In addition to having a negative tetrazolium blue test, those with defects in NADPH oxidase will have negative _______________.

A

dihydrorhodamine tests (i.e., decreased green fluorescence in flow cytometry)

80
Q

Hyperacute graft rejections are type _________ hypersensitivity reactions.

A

II (meaning they have to have preformed antibodies to the transplant)

81
Q

Histologically, what will you see in acute transplant rejections?

A

Dense CD8+ infiltrate in vessels of organs leading to vasculitis

82
Q

What type of hypersensitivity reaction is chronic transplant rejection?

A

II and IV

That is, antibodies and CD4+ T cells develop after transplantation.

83
Q

What histologic pattern is common in chronic organ transplant rejection?

A

Obliterative fibrosis (of lungs, kidneys, and liver–the last of which can show disappearing bile duct syndrome)

84
Q

Which two organ transplantations most often lead to graft-versus-host disease?

A

Liver (rich in lymphocytes) and bone marrow (really rich in lymphocytes, hehe)

85
Q

Cyclosporine inhibits _____________ which decreases IL-2 transcription.

A

calcineurin (by binding cyclophilin)

86
Q

Cyclosporine : cyclophilin = tacroliums : ________________.

A

FKBP

“TACOs with Fish, Kale, Beef, and Pico”

87
Q

Which immunosuppressive medications are neurotoxic?

A

Tacrolimus and cyclosporine

88
Q

IL-2R stimulates what intracellular mediator?

A

mTOR (which is inhibited by sirolimus)

89
Q

Stimulation of ____________ leads to the activation of calcineurin which then ______________.

A

TCR (CD4 and CD3); dephosphorylates NFAT, allowing it to transcribe IL-2

90
Q

Sirolimus is often used in what organ transplants?

A

Kidneys, because sirolimus is not nephrotoxic

“SiRolimus allows the kidneys to SuRvive.”

91
Q

Which drug acts “upstream” in the sirolimus pathway?

A

Basiliximab and daclizumab –both are IL-2R antagonists

Remember Basil Chang on the pogo stick.

92
Q

Corticosteroids work by inhibiting _____________.

A

NF-kB

93
Q

Azathioprine ultimately inhibits which enzyme?

A

PRPP amidotransferase (which is needed in purine synthesis)

94
Q

________________ reversibly binds to IMP dehydrogenase.

A

Mycophenolate mofetil

95
Q

____________ is associated with invasive CMV infections.

A

Mycophenolate mofetil

96
Q

What’s the difference between filgrastim and sargramostim?

A

filGraSTIM activates G-CSF.

sarGraMoSTIM activates GM-CSF.

97
Q

What does oprelvekin do?

A

It stimulates platelet development.

98
Q

What disorders is rituximab used in?

A

Rituximab is an antibody against CD20 and is thus used in any disorder in which B cells are causing a problem: NHL, RA, ITP, and CLL of B-cell origin.

99
Q

Which antibody targets HER2/neu?

A

Trastuzumab (“tras2zumab”)

100
Q

Which cancers are treated with cetuximab?

A

Colorectal cancers

Note: cetuximab targets EGFR.

101
Q

Etanercept has a similar effect to which antibodies?

A

Infliximab and adalimumab

Etanercept is a decoy TNF-alpha receptor. (“It interCEPTs TNf-alpha.”)

102
Q

Eculizumab can treat which condition?

A

Paroxysmal nocturnal hematuria

Eculizumab is an antibody to C5.

(Think: eCulizumab.)

103
Q

Ustekinumab targets what receptor and is used in which conditions?

A

It targets IL-12 and is used for psoriasis.

Think of USbEKastan with psoriasis all over it. Also, Th1 cells are important mediators of psoriasis.

104
Q

Denosumab mimics what endogenous molecule?

A

Osteoprotegerin

105
Q

High-risk infants with RSV can be given _______________.

A

palivizumab

For LIV VIruZ