Exam II Flashcards

1
Q

Type I Hyper-sensitivity

A

Allergy and Anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Type II hypersensivitity

A

antibody-mediated cytotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Type III Hypersensivitity

A

Immune complex disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type IV Hypersensitivity

A

Delayed-type hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Definition of Type I Hyper-sensitivity. Note cell types and Ig involved.

A

Allergy and Anaphylaxis: Rapidly progressing immune rxn thru antigen binding to surface of Ig-E-coated basophils or mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is atopy?

A

Tendency to develop allergies. Make IgE in response to allergens (normally made in response to parasites)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Does Th1 or Th2 response play a role in Type I HS? Why?

A

Th2 is default pathway in absence of inflammation. Allergens don’t elicit inflammatory responses: IgE production is natural outcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the hygiene hypothesis?

A

D/t decreased exposure to pathogens early in life (which would favor development of Th1-mediated immune responses) Th2-mediated immunity takes over: subsequent production of IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain Development of Anaphylaxis

A

See Slides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Histamine effect in allergy/anaphylaxis

A

Bronchial sm cx and increased vascular permeability. Pre-formed in granules of mast cells / basophils. Short lived effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Protease effect in allergy/anaphylaxis

A

activate matrix metalloproteinases which cleave tissue matrix proteins to cause damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

TNF-alpha effect in allergy/anaphylaxis

A

Promotes inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain the eosinophil chemotactic factor of anaphylaxis

A

Accumulation of eosinophils locally or in bloodstream (systemic anaphylaxis) : attempt to counteract effects of histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Leukotrienes (LTs) in anaphylaxis

A

Most potent substances known that cause sm cx and increased vascular permeability. Released slower than histamine (made, not pre-formed) and has longer effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Role of eosinophils in anaphylaxis

A

Accumulate in nasal and bronchial mucosa in resp allergies and intestinal mucosa during certain worm infestations: attach to worms and release granules containing hydrolytic enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Late Phase Response

A

6-8 hrs after immediate rxn thru secretion of prostaglandins, leukotrienes, chemokines, cytokines by mast cells. 2nd phase of sm cx. Sustained edema. Recruitment of eosinophils and Th2 cells. Remodeling of tissue: sm hypertrophy and hyperplasia. May lead to chronic asthma and assoc. airway hyperreactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Detail mechanisms of Epi Tx for Anaphylaxis

A

Epi binds to beta-adrenergic receptors to cause increase in cAMP. This relaxes cx bronchial sm, tightens endothelial cell junctions (stops fluid loss) and stimulates heart. Only Tx that reverses effect of anaphylaxis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Antihistimine Tx for Anaphylaxis/Allergy

A

Bind to histamine receptors to block further binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cromolyn sodium and/or theophylline Tx for anaphylaxis/Allergy

A

Block degranulation of mast cells / basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Repeated allergen injections as a preventative measure for allergy/anaphylaxis

A

High levels of IgG blocking antibody intercept allergen before it reaches IgE-coated basophils. Th1 response that downregulates the Th2 response. IgE levels decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Omalizumab as Tx for allergy/anaphylaxis

A

mouse anti-IgE antibody. Binds to IgE to prevent it from binding to receptor on basophils and mast cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define Type II Hypersensitivity

A

Type II hypersensitivity is cell destruction mediated by a reaction of antibody to a cell surface bound antigen, which can be intrinsic or an exogenous adsorbed antigen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Extracellular bacteria cause tissue destruction by

A

inducing inflammation and releasing some toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Most effective immunity against extracellular bacteria

A

Innate immunity:
Phagocytosis
Alternative complement pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Main adaptive immunity against extracellular bacteria

A

Humoral immunity

IgG opsonizes and toxin-specific antibodies neutralize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Septic shock

A

due to immune response to extracellular bacteria

Macrophages release TNF and IL-1, causes too high of immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Superantigens

A

some bacterial toxins that bind T-cells and MHC molecules on APC regardless of antigenic specificity
Causes activation of many T-cells, lots of cytokines produced, and septic shock-like condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Disease-causing antibodies from Rheumatic fever

A

cross-reactive antibodies bind to sarcolemma proteins in heart and cause carditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Disease-causing antibodies from Poststreptococcal glomerulonephritis

A

antibodies form immune complexes with bacterial antigens, and lodge in kidney causing nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Intracellular bacteria thrive by

A

living inside macrophages

Are inaccessible to circulating antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Innate immunity to intracellular bacteria

A

Mostly ineffective
Macrophages produce IL-12, which activates NK cells to produce IFN-gamma
IFN-gamma fully activates macrophages, and can destroy some of intracellular bacterai

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Most effective immunity against intracellular bacteria

A

Delayed Type Hypersensitivity (Type IV)
TH1 cells release IFN-gamma & activated macrophages may kill bacteria
If bacteria lives, activated macrophages surround microbes and form a granuloma to prevent spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Extracellular bacteria evade immunity by

A

Varying surface antigens

Polysaccharide capsules which resist phagocytosis and inhibit alternative pathway complement activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Intracellular bacteria evade immunity by

A

Preventing fusion of phagosomes and lysosomes

Scavenge reactive oxygen intermediates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Negative effects of granuloma formation

A

compromise tissue function - esp. in lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

innate immunity against virus

A

Virus infected cell releases Type 1 IFN that upregulates expression of class I MHC and activates NK cells and causes uninfected cells to release enzymes that block viral replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

First line of defense against virally infected cells

A
NK cells
See absence of class I MHC caused by virus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Adaptive immunity important early in virus infection

A

Humoral immunity - if antibodies are present (vaccine)

Antibodies bind to virus to prevent from binding to host cell, opsonize virus, and activate complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Adaptive immunity important during established virus infections

A

CTL’s kill virally infected cells that have virus antigen on class I MHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Viruses evade immunity by

A

altering antigens
prevent class I MHC expression (protects against CTLs)
Killing CD4 T cells (HIV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Main source of innate immunity in fungal infections

A

Neutrophils through phagocytosis (lysosomal enzymes and reactive oxygen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Most important adaptive immunity in fungal infections

A

Th1 mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Innate immunity against parasite infections

A

most parasites have a mechanism to defeat innate immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Helminthic infestations activate

A

IgE and eosinophils during ADCC (Th2 immunity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Parasites evade immunity by

A

antigenic variation, acquired resistance to complement, inhibition of host immune responses, antigen shedding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Mechanism of Type II hypersensitivity

A

Antibody bound to cell activates phagocytosis

Complement and Fc receptor activates leukocytes - inflammation and tissue injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hemolytic disease of newborn

A

Mother makes IgG to Rh antigen expressed by RBC’s of her child
Mother is Rh-neg, baby is Rh-pos
First Rh-pos child stimulates immune response, unaffected
Second Rh-pos fetus RBC’s destroyed by macrophages in spleen and liver after being seen by maternal IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Prevention of hemolytic disease of newborn

A

Anti-Rh antibodies given to mother before she delivers Rh-pos baby
Antibodies bind to fetal cells in mother and remove them, preventing mother from becoming sensitized to Rh-pos RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Non-cytotoxic Type II hypersensitivity reactions

A

Do not destroy cells, but disrupt normal function
Grave’s disease - antibodies to TSH receptor causes overproduction of thyroid hormones
Myasthenia gravis - antibodies to acetylcholine receptor blocks nerve impulse transmission to muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Immune complex disease (Type III hypersensitivity)

A

antibodies form complex with antigens

Recruits complement and Fc receptors and activates leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Immune complex disease induced by

A

Autoimmune disease (SLE or RA), Serum sickness, drug reactions, infectious disease, inhaled allergens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

To develop Type III hypersensitivity immune complexes must

A

be medium-sized
Optimal proportions of antibody and antigen required
Antigen must persist for long periods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Immune complexes are normally cleared from body by

A

RBC CR1 protein binds to C3b and C4b on immune complexes

Immune complexes shuttled to liver and spleen and removed from RBC by macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Delayed-type Hypersensitivity (Type IV)

A

Form of cell-mediated immunity that manifests 24-72 hours after exposure to antigen
Mediated by TH1 cells & requires prior sensitization to antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Contact dermatitis

A

Type IV hypersensitivity

Skin exposure to antigen causes delayed inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Tuberculin skin reaction

A

type IV hypersensitivity
injection of PPD skin test presents antigen to memory T cells
Endothelial cells upregulate VCAM-1 to bind memory T helper cell-expressed VLA-4
T cells migrate to skin & interact with antigen-expressing macrophages
Memory T cells activate and secrete IFN-gamma - amplifies reaction
Large number of macrophages activates - tissue damage & red skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Autologous graft

A

transplanted from a person to same person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Syngeneic grafts

A

transplant between two genetically identical people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Allogeneic graft

A

transplant between two genetically dissimilar people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Xenogeneic graft

A

transplant between members of two different species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Orthotopic transplant

A

graft placed in its normal anatomic location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Heterotopic transplant

A

placed in an anatomically different site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

First set rejection

A

similar to primary immune response

graft rejected in 7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Second set rejection

A

similar to secondary immune response

graft transplanted again rejected in 2-3 days

65
Q

Immunologically privileged sites

A

locations where allogeneic transplant placed without risk of rejection
Anterior chamber of eye, cornea, testes, brain

66
Q

Sympathetic ophthalmia

A

one eye is damaged by trauma and autoimmune response to eye proteins (antigens released from damage) threatens undamaged eye
Requires immunosuppressive therapy to keep undamaged eye - may need to remove damaged eye

67
Q

Different MHC proteins perceived as foreign because

A

MHC is polymorphic - all express particular set of self MHC
During education of thymocytes other MHC proteins are percieved as foreign
Probability two random people express same MHC proteins is small

68
Q

Hyperacute rejection

A

Very fast
Takes place within minutes of attaching graft
Mediated by pre-existing antibodies like anti-ABO blood group antibodies
Untreatable

69
Q

Acute Rejection

A

Takes place within 1 month of transplantation

70
Q

Acute humoral rejection

A

antibody and complement-mediated lysis of graft tissue lead to necrosis of blood vessel walls

71
Q

Acute cellular rejection

A

Cell-mediated lysis of graft tissue by CTL’s, NK cells, and macrophages

72
Q

Acute rejection treated with

A

high immunosuppression

high dose steroid therapy or anti-T cell antibodies

73
Q

Chronic rejection

A

may occur months or years after transplantation
May involve antibody-mediated injury to graft vasculature or DTH reactions
Fibrosis and collagen deposition characteristic

74
Q

Alloreactivity

A

foreign MHC proteins recognized by TCR because foreign MHC proteins mimicks conformation
Alloantigens stimulate CD4 alloreactive T cells to become activated
Alloreactive CD4 T cells provide IL-2 and IFN-gamma to alloreactive CD8 cells to produce CTLs that can lyse graft cells

75
Q

Corticosteroid immunosuppression

A

lyse immature thymocytes, block release of cytokines from macrophages and inhibit leukocyte migration

76
Q

Cyclosporine immunosuppression

A

inhibits IL-2 and IFN-g gene expression, preventing activation of cell-mediated immunity
More effective at inhibiting primary immune responses

77
Q

Graft Vs Host disease

A

differentiates bone marrow transplantation
Acute - necrosis of skin, liver, and GI tract
Chronic - fibrosis in organs causing dysfunction
Both can be fatal

78
Q

Anti-CD3 monocolonal antibodies

A

lowers incidence of GVHD but reduces chance of engraftment

79
Q

For autoimmunity to occur

A

central and peripheral tolerance mechanisms must be breached

80
Q

Factors influencing development of autoimmunity

A

abnormalities of lymphocytes and APC’s
Genetic predisposition
Microbial infections

81
Q

Microbe theory of autoimmunity

A

In absence of inflammation, there is low expression of co-stimulatory molecules & get tolerance of self-reactive T cells
Virus infection causes an inflammatory condition and upregulation of co-stimulatory molecules
T cell activated and start autoimmune process
Microbial protein could be homogolous to human proteins and after virus is gone, immune system will be triggered by self-peptide

82
Q

Autoimmune hemolytic anemia

A

Organ specific autoimmune disease
RBC antibodies produced against RBC membrane protein
Causes RBC lysis or removal in spleen and anemia

83
Q

Goodpasture’s syndrome

A
organ specific autoimmune
Autoantibodies to alpha chain of type IV collagen in lung and kidney
Complement activation (humoral) leads to kidney damage, pulmonary hemorrhage, death
84
Q

Pernicious anemia

A

Organ specific autoimmune
Autoantibodies to intrinsic factor and/or gastric parietal cells
Decreases absorption of vitamin B12 leading to anemia

85
Q

Hashimoto’s thyroiditis

A

Organ specific autoimmune
Causes hypothyroid state
Autoantibodies and autoreactive T cells (cell mediated) to thyroid gland proteins

86
Q

Idiopathic thrombocytopenia purpura (ITP)

A

organ specific autoimmune
Platelets destroyed by autoantibodies to platelet membrane proteins
Purple skin lesions due to epidermal hemorrhage
IVIG can prevent destruction of platelets

87
Q

Vitiligo

A

organ specific autoimmune

depigmentation of skin by destruction of melanocytes

88
Q

Grave’s disease

A
organ specific autoimmune
Autoantibodies against TSH receptor
Causes hyperthyroidism (overstimulus of thyroid receptor)
89
Q

Myasthenia gravis

A

organ specific autoimmune
autoantibodies to alpha chain of nicotinic acetylcholine receptor on skeletal muscle cells
Blockage of neuromuscular transmission leading to weakness and paralysis

90
Q

Type 1A diabetes

A

organ specific autoimmune
autoantibodies to insulin-secreting beta-cells in pancreas (used to detect)
Decrease in insulin and increase in blood glucose
Damage caused by CTLs

91
Q

Multiple sclerosis

A

organ specific autoimmune
Demyelinating disease of CNS
TH1 and TH17 cells specific for myelin antigens activated - macrophage activation and damage to myelin-containing nerve cells

92
Q

Systemic Lupus Erythematosus

A

systemic autoimmune
multisystem disease - many autoantibodies (DNA, RNA, proteins)
Broad loss of regulatory control
Most organ systems affected - skin, joints & kidney most common
Type III hypersensitivity major problem (immune complexes)

93
Q

Rheumatoid arthritis

A

systemic autoimmune
Progressive inflammatory disease of joints - destruction of joint cartilage
Inflammation of synovium

94
Q

Treatments to rheumatoid arthritis

A

something that binds up or uses TNF-alpha

95
Q

Sjogren’s syndrome

A

systemic autoimmune
Dry eyes and dry mouth - destruction of lacrimal and salivary glands
B and T cell influx to glands

96
Q

Scleroderma

A

systemic autoimmune
excessive deposition of collagen
T cells inflitrate dermis - release of IL-1 and TNF alpha leads to production of collagen

97
Q

Polymyositis-Dermatomyositis

A

systemic autoimmune

muscle injury brought about by CD4 and CD8 T lymphocytes inflitration of muscles

98
Q

B cell deficiency

A

decreased serum Ig levels
Germinal centers decreased or absent
Susceptible to infection by extracellular bacteria

99
Q

T cell deficiency

A

Decreased skin test reactions (memory), normal or reduced serum Ig levels
Normal follicles, decreased paracortical regions
Susceptible to infection by virus, intracellular bacteria, or fungi

100
Q

X-linked Agammaglobulinemia

A

Bruton’s
Absence of mature B cells - little serum Ig
Pre-B cells exist in bone marrow - block at maturation
Mutations in B cell tyrosine kinase
infections from pyogenic bacteria

101
Q

Common Variable Immunodeficiency

A

Mature B cells can’t differentiate into plasma cells - decreased antibodies
Mature B cells seen

102
Q

Selective IgA deficiency

A

Common - inherited or acquired
Missing IgA antibodies, have rest
Asymptomatic, some infection of mucosa
IgM compensate for missing IgA - J-chain binds to receptor and transported across epithelial cells
Can have anaphylactic if given transfusion or breast milk containing IgA

103
Q

Hyper IgM syndrome

A

overabundance of IgM antibody & lack of others
X-linked hyper IgM - deficiency of CD40L on T cells - no isotype switching (Tcell problem not B cell problem)
Hyper IgM type 2 - utation in gene activation-induced cytidine deaminase prevents isotype switching

104
Q

DiGeorge syndrome

A

Deficiency of T cells
hypoplasia or agenesis of thymus
Defective maturation of T cells - poor CMI against viruses and fungi
T cell function increases with age if keep child healthy

105
Q

SCID

A

Failure of B and T cells to develop from bone marrow stem cells
Little or no humoral or cell-mediated immunity
Deficiency is adenosive deaminase - leads to toxic buildup that kills B/T cells
RAG1/RAG2 deficiency - failure of VDJ rearrangement
X-linked SCID - mutation in gene for cytokine receptors

106
Q

Chronic Granulomatous disease

A

Defect in NADPH oxidase - neutrophils can’t produce superoxide anion during respiratory burst
Increased bacterial infections
Fatal
Interferon-g therapy can prompt neutrophils in some to start producing NADPH oxidase

107
Q

Myeloperoxidase deficiency

A

Decreased or absent myeloperoxidase, HOCl can’t be made from hydrogen peroxide
Compensatory immune mechanisms take place
Can be susceptible to fungal infections

108
Q

Chediak Higashi syndrome

A
Recurrent bacterial infections
lysosomes fuse in neutrophils reducing ability to kill microbes - T cell and NK function imapired
Platelet abnormalities - bleeding
impaired vision
Treat with bone marrow transplant
109
Q

Leukocyte adhesion deficiency

A

Defect in beta chain of LFA-1 and Mac-1 adhesion molecules
Neutrophils can’t adhere to endothelial cells for extravation
Bacterial and fungal infections
Wound healing problems - cant traffic to wound
Fatal without bone marrow transplant

110
Q

Neutropenia

A

mutation in neutrophil elastase enzyme that leads to build-up of toxic intracellular protein - kills neutrophils

111
Q

Wiskott-Aldrich Syndrome

A

Immunodeficiency, eczema, thrombocytopenia

Near normal T and B cell levels - respond poorly to antigen, cannot traffic to sites of inflammation

112
Q

Ataxia - Telangiectasia

A

immune defects, loss of ability to coordinate muscles, vascular lesions, tumors
Decreased T cells and serum IgA, IgE, IgG

113
Q

Tumor Specific Antigens

A

antigens unique to particular tumor and not present on normal cell types
Point mutations or gene rearrangements
Immune response targets - altered self proteins

114
Q

Tumor Associated antigens

A

antigens shared by different tumors, also found on normal tissues
Not therapeutic targets - could kill normal cells

115
Q

Oncogenic viral antigens

A

Some RNA/DNA viruses cause tumors and viral antigens on class I MHC

116
Q

Differentiation antigens

A

tissue specific antigens

Aid in diagnosing certain tumors - revel tissue of origin

117
Q

Anti-tumor CTL

A

against carcinomas, sarcomas, and virus-induced tumors
Most effective against virus induced tumors
Respond to MHC class I

118
Q

Anit-tumor NK cells

A

lyse tumors of hematopoietic origin and virus induced

IFN, TNF-a, IL-2

119
Q

Lymphokine-activated killer (LAK) cells

A

enhanced killing of various tumor cell types as well as broadened tumor recognition

120
Q

Anti-tumor macrophages

A

ADCC or release of TNF-alpha

Lyse tumor cell or cause hemorrhagic necrosis of tumor blood supply

121
Q

Tumor evasion strategies

A

Lack of MHC expression
Induce tolerance - no co-stimulatory molecules
Anti-tumor antibodies could bind to tumor cell and act as blocking factor
antigens shed by tumor cells bind to cell surface receptors
Encase themselves in collagen and fibrin

122
Q

Immunoconjugates

A

antibodies coupled to toxic substance
Endocytosed by tumor cell - kills tumor cell
Fab fragments to avoid non-specific binding

123
Q

Bi-specific antibodies

A

genetically-engineered antibodies that recognize tumor antigens and immune system cells (like T cells)

124
Q

IFN-alpha cytokine therapy

A
tumor antiproliferative effects, increase NK cells, increase class I MHC expression
little side effects
125
Q

Adoptive cellular immunotherapy

A

Lymphokine-activated killer cells

Tumor inflitrating lymphocytes

126
Q

Acute HIV

A

2-6 weeks after initial infection
resembles flu
active virus replication occurs in blood and CSF

127
Q

Asymptomatic HIV infection

A

latent phase
HIV undetectable in blood, replicating in lymphoid tissue
up to 10 years to become active

128
Q

AIDS- related complex (ARC)

A

persistent fevers, night sweats, weight loss, oral candidiasis, chronic mucocutaneous herpes simplex infection
In some patients - die of AIDS more quickly (carry high viral load)

129
Q

AIDS

A

recurrent infections with opportunistic pathogens
Tumors
Progressive wasting syndrome (cachexia) - caused by TNF-a
Dementia
CD4 count drops below 200 cells/cubic mm

130
Q

R5 viruses

A

HIV variants that use CCR5 chemokine receptors

expressed on macrophages and memory T cells

131
Q

R4 viruses

A

HIV variants that use CXCR4 chemokine receptors (T cells)

132
Q

HIV infectious process

A

Plasma membrane-expressed gp120 binds to CD4 and chemokine receptors - initiates membrane fusion and pass HIV genomes to uninfected cells
Once in cell, viral replication or proviral state takes place - integrate vRNA into host DNA with reverse transcriptase

133
Q

NFkB and SP1 transcription factors

A

bind HIV long terminal repeats- control viral gene transcription
activated by cytokines
TNF-a and IL-2 in T cells, IL-1, IL-3, IL-6, TNF-a, IFN-g, and GM-CSF in monocytes and macrophages

134
Q

HIV kills T cells by

A

direct lysis by budding HIV -loose too much membrane
Virus production interferes with cellular protein synthesis
Syncytia formation of infected and uninfected cells
ADCC response
CTL-mediated destruction of virus-infected cells

135
Q

HIV Nef protein

A
downregulates expression of class I MHC - make cell invisible to CTL
Without Nef gene, won't progress to AIDS
136
Q

ELISA

A

screening technique for antibodies
Can be detected 6-9 weeks after infection
High false positive rate - cross reactive antibodies to H-9 antigens

137
Q

Western Blot

A

viral antigens separated
Determines viral proteins to which individual has produced antibodies
Confirmatory test

138
Q

PCR

A

very sensitive
detects viral genomes (DNA) integrated into cell DNA
Used to determine whether neonates have been infected with HIV from mother (checks viral antigen instead of antibody - could have mom’s antibodies)

139
Q

RT-PCR

A

detects free virus in body fluids
Uses reverse transcriptase to convert viral RNA to DNA
Used to assess viral loads in adults

140
Q

Ideal vaccine

A
no undesirable side effects
easy to administer
highly immunogenic
highly protective
long-term immunity
141
Q

Attenuated vaccines

A

Live virus - weakened from living in non human host
Sabin polio vaccine, measles, mumps, rubella, yellow fever
Attacks with humoral and CMI
Long lasting immunity but can have full virulence

142
Q

Don’t give attenuated vaccines to

A

Immunocompromised or pregnant women

143
Q

Inactivated viral vaccine

A

Influenza, rabies, polio (Salk) viruses

Less concern for safety, but don’t generate same level of protection

144
Q

Subunit viral vaccines

A

single viral protein
Hep B surface antigen
uses only piece of virus

145
Q

Inactivated bacterial vaccines

A

not used anymore - bad side effects

146
Q

Toxoid bacterial vaccines

A

detoxified bacterial toxins

Diptheria and tetanus toxoids in DTaP

147
Q

Conjugate bacterial vaccine

A

polysaccharide attached to protein carrier to produce high affinity IgG and memory reponse

148
Q

Adjuvants

A

added to vaccine to get better immune response

149
Q

Hepatitis B vaccine

A

Protein grown in yeast

Serum antibody prevents virus from infecting liver

150
Q

Diphtheria, tetanus, acellular pertussis vaccine (DTaP)

A

D/T toxoids and acellular pertussis

Protects against toxins, won’t eradicate bacteria

151
Q

Hemophilus Influenzae type B vaccine

A

causes Meningitis
Conjugate vaccine - T cell-dependent immune response with IgG - kill disease in blood stream before getting to brain
First conjugate vaccine

152
Q

Meningococcal vaccine

A

protects against Neisseria memingitidis - causes meningitis

Conjugate vaccine

153
Q

Polio Vaccine

A

Use inactivated Salk poliovirus (IPV) instead of live (OPV)

kills virus in blood before getting to CNS

154
Q

MMR

A

protects against Mumps, Measles, Rubella (protect fetus from rubella)
Live, attenuated vaccine - antibody and CMI

155
Q

Varicella vaccine

A

protects from chicken pox
Live, attenuated viral vaccine
antibody + CMI

156
Q

Rotavirus vaccine

A

Rotavirus - diarrheal pathogen in children

Tetravalent rhesus-human reassortant - uses attenuated rhesus virus expressing human virus VP7 antigen

157
Q

Pneumococcal vaccine

A

disease causes meningitis

Conjugated vaccine

158
Q

Influenza vaccine

A

live attenuated - flumist OR inactivated

Contains two different influenza A virus, one influenza B virus

159
Q

HPV vaccine

A

protects against HPV - cancer

L1 protein-expressing virus-like particles