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Immunology Block > Final week > Flashcards

Final week Flashcards

1
Q

Define Self-antigens:

A

An individual own antigens (blood type antigens)

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2
Q

Define immunologic tolerance:

A

Unresponsiveness to self-antigens (negative selection process)

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3
Q

Define tolerogens:

A

Antigens that induce tolerance

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4
Q

Define Immunogens:

A

Antigens that induce an immune response

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5
Q

Define Autoimmunity:

A

Failure of self-tolerance and resulting immune reaction to self-antigens

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6
Q

What is central tolerance?

A
  • Immature developing lymphocytes encountering self-antigens in generative lypmhoid organs
  • T cells: deletion and regulatory T cells
  • B cells: receptor editing, deletion, anergy
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7
Q

What is peripheral tolerance?

A
  • Mature lymphocytes encounter self-antigens in secondary lymphoid organs
  • T cells: anergy, suppression, deletion
  • B cells: anergy, suppression, deletion
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8
Q

What are the 2 main pathways for central tolerance in T cells?

A
  • Negative selection (deletion)
  • Development of regulatory T cells
  • The tolerance of T cells usually influences B cell tolerance
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9
Q

Where do DN thymocytes enter the thymus?

A

Right at the border of the medulla, where they then venture into the cortex for maturation

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10
Q

What is AIRE?

A
  • AutoImmune Regulator Protein (AIRE)
  • Expressed in thymic medullary epithelial cells
  • Presents peripheral tissue antigens to thymus
  • Without AIRE, there is no regulation and autoimmunity results!
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11
Q

What is APECED and its classic triad?

A
  • Autoimmune PolyEndocrinopathy Candidiasis Ectodermal Dystrophy
  • Classic Triad: mucocutaneous candidiasis, adrenal insufficiency, and hypoparathyroidism
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12
Q

What is the mode of inheritance for APECED?

A
  • Autosomal recessive
  • Mutations in AIRE gene
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13
Q

Which T cells do not depend on AIRE for their development?

A

Regulatory T cells

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14
Q

Where is icos expressed and what is its function?

A
  • Expressed on activated T cells
  • Costimulation of T cells & generation of T follicular helper cells
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15
Q

Where is CTLA-4 expressed and what is its function?

A
  • Activated T cells
  • Negative regulation of immune response & self-tolerance
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16
Q

Where is PD-1 expressed and what is its function?

A
  • T cells, B cell, and myeloid cells (activated)
  • Negative regulation of effector T cells & self tolerance
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17
Q

What are the two forms of T cell anergy?

A

After recognition of self-antigen

  • Signaling block
  • OR
  • Engagement of inhibitory receptors
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18
Q

What is CD25?

A

Alpha chain for IL2 receptor

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19
Q

What is the difference between natural and induced T regs?

A
  • Natural develop in the thymus
  • Induced develop in the peripheral tissues (TGF-beta)
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20
Q

What are the 3 main ways T regs suppress the immune response?

A
  1. Production of inhibitory cytokines (IL-10 & TGF-beta)
  2. Expression of CTLA-4
  3. Expression of IL-2 receptor and capture of IL-2
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21
Q

What is IPEX and its classic triad?

A
  • Immune Dysregulation, Polendocrinopathy, Enteropathy, X-linked Syndrome
  • Classic Triad: enteropathy (diarrhea), dermatitis (eczema), endocrine disease (diabetes/thyroid)
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22
Q

What is the difference between intrinsic and extrinsic in peripheral T lymphocyte deletion?

A
  • Intrinsic- cell death caused by deficiency of survival genes (mitochondria releases inducers of apoptosis)
  • Extrinsic- cell death caused by engagement of death receptors (FasL and Fas interaction)
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23
Q

What is ALPS and its common mutations?

A
  • Autoimmune Lympho-Proliferation Syndrome
  • Disorder of apoptosis
  • Dominant mutation: Fas, FasL, caspase 8, caspase 10
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24
Q

Which antigens are nonprotein and T-independent?

A
  • Polysaccharides
  • Lipids
  • Nucleic Acids
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25
Q

What immunoglobulin isotype responds to T-independent antigens?

A

IgM (short-lived plasma cells)

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26
Q

What are the pathways for central B cell tolerance?

A
  • If self-reactive, can form new light chain to avoid
  • If self-reactivity continues, apoptosis
  • If responds to self-antigen with low-avidity, it can enter anergy
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27
Q

What are the two main forms of peripheral B cell tolerance?

A
  • Anergy and deletion (in absence of T cell co-stimulation)
  • Regulation by inhibitory receptors
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28
Q

What are the common steps in autoimmunity development?

A
  1. Inheritance of susceptibility gene and failure of self-tolerance
  2. Tissue injury and inflammation
  3. Activation of tissue APCs and self-reactive lymphocytes
  4. Self-reactive effector lymphocytes cause tissue injury
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29
Q

What are some common polymorphisms (Non-HLA) and their associated autoimmune disease?

A
  • PTPN22 (RA and others)
  • NOD2 (Crohn’s Disease)
  • CD25 (MS, Type 1 diabetes, others)
  • C2, C4 (SLE)
  • FCGRIIB (SLE)
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30
Q

What are some single-gene defects that cause autoimmunity?

A
  • AIRE (APECED)
  • Foxp3 (IPEX)
  • FAS (ALPS)
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31
Q

What are the 2 main form of environmental factors that lead to autoimmunity?

A
  1. Induction of costimulators on APCs
  2. Molecular mimicry
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32
Q

In what disease are both B lymphocyte and T lymphocyte tolerance defective?

A

Systemic Lupus Erythematosus

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33
Q

What are some common environemntal factors associated with SLE?

A
  • UV radiation
  • Viral infection
  • Drugs and chemicals
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34
Q

What are some common Anti-__ antibodies involved in SLE?

A
  • Antinuclear antibody
  • Anti-dsDNA antibody
  • Anti-Smith antibody
  • Anti-Ro (SSA) antibody
  • Anti-La (SSB) antibody
  • Anti-RNP antibody
  • Anti-histone antibody
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35
Q

A malar rash is associated with what disease?

A

Lupus

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36
Q

What hormonal factors are associated with SLE?

A
  • Increased in women during child bearing years
  • Estrogen-induced flares
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37
Q

Define hypersensitivity

A

Overreaction of normally protective response that results in tissue injury and disease

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38
Q

What are the 3 common triggers of hypersensitivity?

A
  • “self” antigens- autoimmunity
  • Microbial antigens- excessive inflammation
  • Environmental antigens- allergy/atopy
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39
Q

What is the most common type of hypersensitivity?

A

Type 1

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40
Q

How is type 1 hypersensitivity characterized?

A
  • Allergy or atopy
  • Rapid onset (minutes)
  • Antigen-specific IgE
  • Mast cell (histamine) and eosinophil involvement
  • Vasoactive mediators, lipid mediators, cytokines
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41
Q

What are some common examples of Type 1 hypersensitivity?

A
  • Allergic rhinitis
  • Atopic asthma
  • Anaphylaxis
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42
Q

What antibodies mediate type 2 and 3 hypersensitivity?

A

IgG and IgM

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43
Q

Which type(s) of hypersensitivity often involve auto-antibodies or foreign antigens?

A

Type 2 and 3

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44
Q

What is the role of the antibodies in type 2 hypersensitivity?

A
  • Antibody directly binds the target
  • Antigens are specific cells or extracellular matrix
  • Local, tissue specific
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45
Q

What is the role of the antibodies in type 3 hypersensitivity?

A
  • Immune complex deposition
  • Antigens present in circulation
  • Systemic
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46
Q

Which class of immunoglobulins has the most subtypes?

A
  • IgG (1-4)
  • IgA has 2 subtypes
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47
Q

How is type 2 hypersensitivity characterized?

A
  • Cytotoxic hypersensitivity
  • Onset in minutes-hours
  • Complement and Fc receptor mediated (involves opsonization/phagocytosis or hormone signaling)
  • Neutrophils can cause direct tissue injury
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48
Q

What are some examples of Type 2 hypersensitivity?

A
  • Goodpasture’s Syndrome
  • Idopathic thrombocytopenic purpura (ITP)
  • Autoimmune hemolytic anemia (AIHA)
  • Grave’s (antibody stimulates TSH receptor)
  • Myasthenia gravis (antibody inhibits Ach receptor)
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49
Q

In what disease are antibodies against the basement membrane of the kidney and lung made?

A

Goodpasture’s syndrome (type 2)

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50
Q

How is type 3 hypersensitivity characterized?

A
  • Immune complex hypersensitivity
  • Onset within hours
  • Complement and Fc receptor mediated
  • Complexes deposited in vascular basement membrane
  • Lysosomal enzymes and ROS cause damage, neutrophils (vasculitis)
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51
Q

What is “serum sickness”?

A
  • A type 3 hypersensitivity response
  • Body makes antibodies against foreign antibodies (diptheria and horse antibodies)
  • Complex formation and deposition causes symptoms (fever, hives, joint pain)
52
Q

How is type 4 hypersensitivity characterized?

A
  • Delayed type hypersensitivity
  • Onset of hours to days
  • Involved CD4+ and CD8+ T cells, macrophage activation, and direct target cell lysis
  • Non-transferrable by serum (not antibodies)
53
Q

What are some examples of Type 4 hypersensitivity?

A
  • Poison ivy contact dermatitis (urushiol is lipid soluble and is presented on MHC 1 molecules)
  • TB test
54
Q

What are some examples of type 3 hypersensitivity?

A
  • SLE
  • Serum sickness
  • Vasculitis
55
Q

What are the general steps that lead to immediate hypersensitivity?

A
  1. First exposure to antigen (activate Th2 cells and stimulate IgE class switch in B cells)
  2. Production of IgE & binding to mast cells (FcR)
  3. Repeat exposure to antigen
  4. Activation of mast cell (release mediators)
  5. Immediate reaction (minutes after repeat exposure)
  6. Late Phase Reaction
56
Q

What is the role of IgE in hypersensitivity?

A
  • Sensitize mast cells
  • Recognition of antigen
57
Q

What is the difference between immediate and late phase response in hypersensitivity reaction?

A
  • Immediate- minutes after exposure and result of vasoactive amines/lipid mediators
  • Late- happens a few hours after exposure and result of cytokine release
58
Q

Where are mast cells mainly located?

A

GI tract, skin, and respiratory

59
Q

What is a pruritic rash?

A

Itchy rash (allergic response)

60
Q

What are the most common food allergies?

A
  • Milk, egg, peanut, wheat, soy
  • To a lesser extent: fish, shellfish, tree nuts
61
Q

What are common candidate genes that cause asthma?

A
  • Cytokine gene clusters (IL4, IL5, IL13), CD14, and B-adrenergic receptor
  • ADAM33
62
Q

How does ADAM33 cause asthma?

A

Metalloproteinase involved in airway remodeling

63
Q

What is a gene candidate for atopic dermatitis?

A

Filaggrin- component of terminall differentiated keratinocytes important for epithelial barrier function

64
Q

What are the general steps in mast cell activation?

A
  1. IgE coating (occurs on Fc receptor)
  2. Antigen activated mast cell (needs cross-linking of antigen & IgE-FcR)
  3. Histamine/lipid mediators (immediate)
  4. Cytokines (late)
65
Q

What is systemic anaphylaxis?

A

Systemic immediate hypersensitivity reaction characterized by edema in many tissues & decrease in blood pressure (secondary to vasodilation)

66
Q

What is a wheal and flare reaction?

A
  • Result of intradermal injection of antigen
  • Vasodialation on edge of lesion
  • Vasodilation and congestion in “wheal” (mast cells, edema)
67
Q

What is the value of a skin prick test (or in vitro serum test)?

A

Excellent negative predictive value (positive predicitive value is ~50%)

68
Q

Who are “atopic” individuals?

A
  • Susceptible to immediate hypersensitivity
  • Have more IgE in blood and more IgE-specific Fc receptors per mast cell
69
Q

How are eosinophils recruited and activated?

A
  • Recruited by chemokines and IL4
  • Activated by IL5
70
Q

What is the role of biogenic amines and lipid mediators?

A

Rapid vascular and smooth muscle reactions (vasodilation, vascular leakage, edema, brochoconstriction, gut hypermotility)

71
Q

Is asthma an immediate or late-phase reaction?

A

Both

72
Q

Is susceptibility to allergic disease inherited?

A

Yes

73
Q

What are Eicosanoids?

A
  • Made by oxidation of 20C FA
  • Inflammation and Immunity processes
  • Include prostaglandins and leukotrienes
74
Q

What is the main precursor for Eicosanid synthesis?

A

Arachidonic Acid (synthesized by Phospholipase A2)

75
Q

What enzyme is used to synthesize Leukotrienes from Arachidonic acid?

A

Lipoxygenase

76
Q

What enzyme is used to synthesize prostaglandins and thromboxanes from Arachidonic acid?

A

Cyclooxygenase (COX)

77
Q

What is the difference between COX-1 and COX-2?

A
  • COX-1: Constitutive expression, ubiquitis location, “houskeeping” functions
  • COX-2: Inducible (pro-inflammatory signals), Inflammatory site location, proinflammatory functions
78
Q

What is the downside of Cox inhibitors?

A
  • Cox inhibitors are used to decrease inflammtory response
  • However, most of the drugs act on both Cox-1 and Cox-2 (causing GI problems)
  • Need Cox-2 selective drugs!
79
Q

What is the mechanism of NSAIDs?

A

Inhibition of prostraglandin production and interferes with physiological roles of molecules

Frequently leads to erosion of GI mucosal protection

80
Q

What is the generic name of Aspirin and its MoA?

A
  • Acetylsalicylic acid
  • Transfers functional group onto COX enzyme (irreversible inhibition)
  • Leukotriene pathway remains unaffected
81
Q

What are some of the major problems with aspirin use?

A
  • GI disturbance (direct effect on mucosa)
  • Prolonged bleeding (decreased platelet function for 4-6 days)
  • Tinnitus (aspirin toxicity)
82
Q

What is the relationship between therapeutic effects and dose in aspirin?

A
  • Low dose (30-100mg): antiplatelet
  • Medium dose (.3-.6g): analgesic and antipyretic
  • High dose (3-5g): anti-inflammatory
83
Q

What is Kawasaki disease?

A
  • Persistenet fever with increased risk of CAD (must meet criteria)
  • Risk of vasculitis
  • Treatment is IVIG with aspirin (initially high dose, then low)
84
Q

What is Reye’s Syndrome?

A
  • Result of giving aspirin to lower fever following viral infection
  • Five clinical stages (lead to coma and seizure)
  • Use ibuprofen or acetaminophen instead
85
Q

What are the signs of acute vs chronic poisoning with aspirin?

A
  • Acute- respiratory depressoin and acidosis
  • Chronic- Nausea, tinnitus, hyperglycemia
86
Q

What is it called when aspirin leads to nasal congestion and acute, sever bronchospasm?

(also increased risk for anaphylaxis and angiodema)

A

Aspirin Sensitive Asthma

87
Q

What is the most frequently used and quickest acting NSAID?

A
  • Ibuprofen
  • Sold as: advil, motrin, nuprin
  • Also has longer duraction of action compared to acetaminophen
88
Q

What are some properties of Ibuprofen?

A
  • Peak plasma levels in 15-30 minutes
  • Half-life of about 2 hours
  • Anti-inflammatory regimen requires 2400-3200mg daily
  • Take with food (GI problems)
89
Q

What drug is chemically similar to Ibuprofen with a longer half-life?

A
  • Naproxen (Naprosyn, Aleve)
  • Half-life of about 12 hours (take twice a day)
  • Peak plasma within 2-4 hours
  • Higher rate of GI bleeding
90
Q

What is Indomethacin (Indocin) mainly used to treat?

A

Gout (has sever side effects, so not much else)

91
Q

What is the significance of Nabumetone (Relafen)?

A
  • Only nonacid NSAID currently available
  • Take once-a-day (halflife 24 hours)
92
Q

What is the significance of Rofecoxib (Vioxx)?

A
  • Highly selective COX-2 inhibitor
  • Taken off market in 2004 due to increased risk of MI and stroke
93
Q

What is the significance of Celecoxib (Celebrex)?

A
  • COX-2 inhibitor
  • Does not appear to cause more heart problems
94
Q

What is the significance of Ketorolac (Toradol)?

A
  • Only NSAID for IM or IV injection
  • Used mainly in postoperative patients
  • Risk of renal effects
95
Q

How to Corticosteroid drugs suppress the immune system?

A
  • Regulate the transcription of molecules
  • Increase lipcortin
  • Decrease IL1, IL2, TNF-alpha, INF-gamma
96
Q

What are the two pathways of corticosteroid effects on Eicosanoid production?

A
  • Decrease the activity of Phospholipase A2 (by increasing Lipocortin)
  • Decrease the expression of COX-2
97
Q

What part of the immune response to glucocorticoids affect most?

A
  • There is more inhibition of the cell-mediated arm over the humoral arm
  • Also induce apoptosis in rapidly-dividing leukocytes
98
Q

What are some of the common uses corticosteroids?

A
  • Graft rejection and delayed hypersensitivity
  • Transplant rejection
  • suppress hypersensitivity/allergies
99
Q

What is one of the negatives of corticosteroid use?

A
  • Increase risk of infection (espcecially CMI)
  • Cannot use live virus vaccines during regimen
  • Longterm use can cause Cushing’s Syndrome (fat face)
  • Impaired wound healing
100
Q

Do NSAIDs ameliorate the ongoing immune reaction?

A

No, just address the symptoms

101
Q

Is acetaminophen an NSAID?

A

No, because it does not decrease inflammation

102
Q

What is RICEM and when is it used?

A
  • Rest
  • Ice
  • Compression
  • Elevation
  • Medication (anti-inflammatory)

Use with acute inflammation caused by trauma!

103
Q

What is he main problem with the results and science behind herbals?

A

Most only show in vitro activities

104
Q

What is one of the exceptions to the problem with herbal supplement studies for inflammation?

A

Cat’s claw has clinical trials showing improvement of osteoarthritis

105
Q

What are the 3 main mechanisms for immunosuppressant drugs?

A
  1. Cytotoxic (cause cell death)
  2. Inhibit proliferation or fxn of lymphocytes
  3. Prevent lymphocyte proliferation (via nucleotides)
106
Q

What does DMARDS stand for?

A
  • Disease Modifying Anti-Rheumatic Drugs
  • RA is a systmic inflammatory disease
107
Q

What is Methotrexate MoA, usage, and adverse effects?

A
  • Inhibits DHFR (folate metabolism)-> no DNA
  • Use high dose in chemo, low dose in autoimmune
  • Can cause liver and bone marrow effects
108
Q

What is the MoA, usage, and adverse effects in Mycophenolate Mofetil (CellCept)?

A
  • Inhibits IMPDH (purine/DNA synthesis)
  • Used to prevent graft rejection and for autoimmune
  • Can effect GI and bone marrow
109
Q

What is the difference between conventional and biologics as immunosuppressant drugs?

A
  • Conventional- interfere with combinations of pathways
  • Biologics- selectively inhibit a cytokine or receptor
110
Q

What immunosuppressants are used to prevent transplant rejection, but not in kidneys due to nephrotoxicity?

A
  • Cyclosporin and Tacrolimus
  • Both are calcineurin inhibitors and prevent IL2 transcription
111
Q

What immunosuppressant is an mTOR inhibitor that can cause cytopenias?

A
  • Sirolimus
  • Prevents IL2 response
  • Used to prevent renal transplant rejection
112
Q

What immunosuppressant blocks nucleotide synthesis and can cause cytopenias?

A
  • Azathioprine (Imuran)
  • Inhibits lymphocyte proliferation
  • Prevents transplant rejection, RA, Chrohn’s
113
Q

How do glucocorticoids prevent transplant rejection?

A

Inhibit NFkB (which decreases cytokine transcription)

114
Q

What is a biologic that ends with -ximab?

A

Chimera (mostly human, but mouse derived)

115
Q

What is a biologic that ends with -zumab?

A

Mostly human (humanized!)

116
Q

What is a biologic that ends with -umab?

A

100% human

117
Q

Which biologic targets the Jak1/Jak3 pathway?

A

Tofacitinib (Xeljanz)

118
Q

Why is Etanercept (Enbrel) not considered a mAb?

A

Because it is a man made fusion protein

119
Q

What do Etanercept (Enbrel), Infliximab (Remicade), Adalimumab (Humira) all inhibit?

A

TNF-alpha

120
Q

What is Sreptococcus pyogenes (GABHS)?

A
  • Group A Beta Hemolytic Streptococcus
  • Causes acute rheumatic fever
121
Q

What is one of the big concerns with acute rheumatic fever (ARF)?

A
  • Inflammation of the heart, joints, brain, and vascular connective tissue
  • Due to cross-reactive antibody and/or CMI
  • Treat with corticosteroids (Salicylates too)
122
Q

What is autoinflammatory disease?

A
  • Errors in innate immune system
  • Perioidic fever, joint pains, abdominal pains
  • Common in USA is PFAPA
123
Q

What kind of immune reaction if caused by TH2 activation?

A

Humoral immunity (not CMI)

124
Q

What kind of response does a live virus vaccine cause?

A

A CD8+ T cell response (this will be intracellular processing)

125
Q

What is the classic sign of Chediak-Hegashi Syndrome?

A

Giant cytoplasmic granules in mononuclear cells

126
Q

What do you call the atypical lymphocytes reacting to the EBV-infected B cells?

A

Downey cells (CD8+ T cells target them infected B cells)

Immunology Block (6 decks)

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