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Immunology-Spring 2017 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What are hypersensitivity/allergic reactions?

A

Adaptive immune responses to innocuous environmental antigens

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2
Q

What are allergens?

A

Antigens that cause allergic reactions

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3
Q

What is IgE involved in?

A

Defense against parasites and type I hypersensitivity reactions

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4
Q

In developing countries, what do IgE responses do?

A

Protect against helminth infections

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5
Q

In developing countries, what is the prevalence for allergies?

A

Low

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6
Q

In developed countries, what are IgE responses responsible for?

A

Type I hypersensitivity reactions

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7
Q

What are IgE responses directed at in developed countries?

A

Innocuous environmental antigens

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8
Q

Where are mast cells located?

A

In association with blood vessels and at epithelial surfaces

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9
Q

What does the primary exposure to an antigen result in?

A

Activation of Th2 cells and class switching to IgE

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10
Q

What does IgE bind to and do?

A

Binds to mast cells and sensitizes the mast cell to the allergen

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11
Q

What is the process for activation of IgE mediated type 1 allergic reactions? (4)

A

First exposure to pollen
Extraction of antigen
Activation of antigen-specific T cells
Production of IgE and its binding to mast cells

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12
Q

What happens due to the fact that mast cells are long lived?

A

They accrue a diversity of antibodies

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13
Q

What does the cross-linking of mast cell receptors result in?

A

Degranulation

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14
Q

What do mast cells responses act to? (2)

A

Physically expel the pathogen

Recruit and activate other effector cells

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15
Q

What are eosinophils home to?

A

Sites of allergic reactions

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16
Q

When are eosinophils produced in greater numbers?

A

During immune stimulation

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17
Q

What are 2 effector functions of eosinophils?

A

Release cytotoxic molecules to damage pathogen

Amplify inflammatory response

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18
Q

What can the response of a sensitized individual to intradermal allergen or inhaled allergen be divided into?

A

The immediate reaction and the late-phase reaction

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19
Q

What is the immediate reaction due to?

A

Release of pre-formed mast cell inflammatory mediators

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20
Q

What do edema and reddening of skin result in during the immediate reaction?

A

Wheal and flare reaction

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21
Q

What do edema and constriction of smooth muscle result in during the immediate reaction?

A

Airway narrowing

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22
Q

What is the late phase reaction caused by?

A

Continuous synthesis and release of inflammatory mediators

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23
Q

What happens with edema in late-phase reaction?

A

Increased area and degree

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24
Q

What happens with airway narrowing in late-phase reaction?

A

Second phase

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25
Q

What does the symptoms of IgE mediated allergic reactions depend on?

A

The route of entry of the allergen

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26
Q

What are the 5 types of reactions?

A 
Systemic anaphylaxis
Acute urticaria
Seasonal rhinoconjunctivitis
Asthma
Food allergy
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27
Q

What is the route of entry for systemic anaphylaxis?

A

Intravenous

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28
Q

What is the route of entry for acute urticaria?

A

Through skin

Systemic

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29
Q

What is the route of entry for seasonal rhinoconjunctivitis?

A

Contact with conjunctiva of eye and nasal mucosa

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30
Q

What is the route of entry for asthma?

A

Inhalation leading to contact with mucosal lining of lower airways

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31
Q

What is the route of entry for a food allergy?

A

Oral

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32
Q

What are features of allergens that promote activation of Th2 cells that drive IgE production?

A

Allergens are soluble proteins carried on dry particles
Usually derived across mucosal tissue at low dose
Several allergens are proteases

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33
Q

What is allergen capable of on contact with mucus?

A

Diffusing into mucosal tissue

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34
Q

What do allergens contain?

A

Peptides that can bind MHC class II

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35
Q

What is predisposition to allergic disease influenced by?

A

Genetic and environmental factors

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36
Q

What is atopy?

A

A predisposition to mount IgE responses to environmental allergens

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37
Q

How many people may be atopic?

A

Up to 40% of European and North American

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38
Q

What is the hygiene hypothesis?

A

Main candidate environmental factor is changes to exposure of infectious disease in early childhood

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39
Q

What does excess hygiene result in?

A

Less early exposure to common environmental microbes

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40
Q

What may less early exposure to common environmental microbes do?

A

May make the body less efficient at producing immune-modulatory responses

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41
Q

How can allergens be directly injected into the blood?

A

Via insect/animal bites

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42
Q

Can allergens be absorbed into the blood stream?

A

Yes

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43
Q

What do allergens bind to?

A

Mast cells in connective tissues around the body that surround blood vessels

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44
Q

What are symptoms of systemic anaphylaxis like?

A

Mild (such as hives) or fatal (results anaphylactic shock)

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45
Q

What do serious symptoms of systemic anaphylaxis cause?

A

Loss of blood pressure due to loss of fluid (results in shock)
Constriction of airways and swelling of epiglottis (leads to asphyxiation)

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46
Q

What is allergic rhinitis?

A

Mild allergic reaction caused by allergens that enter through the nasal mucosa and activate mast cells below the nasal epithelium

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47
Q

What does allergic rhinitis cause?

A

Local edema
Blocked nasal passages
Increased mucus produciton

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48
Q

What is allergic conjunctivitis?

A

Allergens enter through the conjunctiva and cause watery inflamed eyes

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49
Q

What is asthma?

A

An allergic reaction caused by allergens that activate mucosal mast cells in the respiratory tract

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50
Q

What is the acute response to rhinitis and asthma?

A

Bronchial constriction and an increase in fluid and mucus

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51
Q

What is the chronic response to rhinitis and asthma caused by?

A

Continued presence of TH2 cells, eosinophils, and other leukocytes

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52
Q

What do allergens do when there is urticaria and angioedema?

A

Activate mast cells in the skin and cause raised swellings

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53
Q

What is urticaria?

A

Swelling is at the surface of the skin

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54
Q

What is angiodema?

A

Swelling is in deeper layers of the skin

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55
Q

With food allergies, what can allergens cause?

A

Systemic effects and gut reactions

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56
Q

How many people have a food allergy?

A

Approximately 1-4% of US and European adults

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57
Q

What is the most common food allergy? What percentage does this allergy make up?

A

Peanut allergy

25%

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58
Q

What does food allergens cause?

A

Cramps, vomiting, and diarrhea

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59
Q

What are current treatments for allergic disease?

A

Treat the symptoms or general anti-inflammatory drugs

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60
Q

What is epinephrine used to do?

A

Prevent anaphylactic shock

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61
Q

How does epinephrine work?

A

Stimulate reformation of tight junctions and relaxation of smooth muscle

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62
Q

What do antihistamines do?

A

Relieve symptoms of rhinoconjunctivitis and urticaria

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63
Q

How do antihistamines work?

A

Block histamine receptor

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64
Q

What corticosteroids do?

A

Promote dilation of bronchial smooth muscle

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65
Q

What does monoclonal anti-IgE antibody do?

A

Prevents IgE binding to IgE receptors

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66
Q

What is monoclonal anti-IgE antibody to do?

A

Control chronic asthma

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67
Q

What is Type II hypersensitivity characterized by?

A

An IgG antibody response to allergens that have bound to the surface of host cells

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68
Q

What does IgG do in type II hypersensitivity?

A

Tags the host cells for opsonization and destruction and activates complement

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69
Q

What are type III hypersensitivity response mediated by?

A

An IgG antibody response to an excess of small soluble antigen that forms antigen:antibody immune complexes

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70
Q

In type III hypersensitivity, where are immune complexes formed?

A

Throughout the body

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71
Q

In type III hypersensitivity, where do immune complexes deposit?

A

In blood vessels, lung alveoli, or global

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72
Q

In type III hypersensitivity, what can immune complexes do?

A

Activate complement resulting in an inflammatory response mediated by C3a and C5a

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73
Q

What are type IV hypersensitivity responses mediated by?

A

Allergen specific effector T cells

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74
Q

What are type IV reactions also called?

A

Delayed hypersensitivity reactions

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75
Q

What is an example of type IV hypersensitivity?

A

Allergic contact dermatitis

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76
Q

What is allergic contact dermatitis caused by?

A

Direct skin contact with an allergens

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77
Q

What do allergens do in allergic contact dermatitis?

A

Penetrate the skin and are taken up by antigen presenting cells

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78
Q

What can the allergens in allergic contact dermatitis cause?

A

Activation of CD4 or CD8 T cells

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79
Q

What does the tuberculin skin test mimic?

A

A type IV hypersensitivity

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80
Q

Chapter 14 study guide and charts

A

Chapter 14 study guide and charts

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81
Q

What is an autoimmune response?

A

An immune response against self-antigens

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82
Q

What are autoantigens?

A

Self-antigens that trigger an immune response

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83
Q

What does the immune system normally show?

A

Tolerance to self-antigens

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84
Q

When do autoimmune responses result?

A

When self-tolerance breaks down

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85
Q

How many mechanisms exist to ensure self-tolerance?

A

Several

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86
Q

What do the self-tolerance mechanisms effective at collectively?

A

Preventing autoimmunity

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87
Q

What is a major task of autoimmune responses?

A

To differentiate self from non-self

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88
Q

What does negative selection select against?

A

Lymphocytes that are strongly self-reactive

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89
Q

What do lymphocytes that are weakly reactive to self-antigens do?

A

Escape negative selection

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90
Q

What do many lymphocytes with low self-reactivity recognize?

A

Foreign antigens

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91
Q

If all weakly self-reactive lymphocytes were eliminated, what would happen?

A

Immune response would be impaired

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92
Q

What can weakly reactive lymphocytes potentially produce?

A

Autoimmune disease

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93
Q

When are T-cells activated?

A

When their receptor binds antigen in the presence of co-stimulation from the antigen presenting cell

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94
Q

When are B-cells activated?

A

When their receptor binds antigen in the presence of T cell co-stimulation

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95
Q

What are lymphocytes that bind antigen in the absence of co-stimulation signaled to do?

A

Undergo apoptosis or become anergic

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96
Q

What are some T cells that are strongly self-reactive in the thymus induced become?

A

Tregs

97
Q

What are some T cells that bind antigen in the presence of anti-inflammatory cytokines induced to become?

A

Tregs

98
Q

What can T cells do?

A

Inhibit other effector T cells that recognize autoantigens in the same general vicinity

99
Q

Do Tregs that inhibit other effector cells have to recognize the same antigens?

A

No

100
Q

What could self-reactive lymphocytes encounter?

A

An activated dendritic cells presenting self-antigen and expressing co-stimulatory molecules

101
Q

What may inflammatory cytokine produced during an infection do?

A

Activate DCs

102
Q

What may inflammatory cytokines down-regulate?

A

Treg responses

103
Q

What may the autoantigen be a ligand for?

A

PAMPs

104
Q

What could autoantigens that are ligands for PAMPs do?

A

Activate self-reactive B cells if it reaches an unusually high concentration

105
Q

What do responses of autoimmune disease resemble?

A

Those that target invading pathogens, but the autoantigens often cannot be removed

106
Q

Because autoantigens cannot be removed, what are autoimmune disease like?

A

Chronic

107
Q

What autoimmune diseases affect a specific organ? (4)

A

Type I diabetes
Myasthenia gravis
Graves disease
Multiple sclerosis

108
Q

What autoimmune diseases are systemic?

A

Rheumatoid arthritis

Systemic lupus erythematosus

109
Q

What are mechanisms of tissue injury analogous to?

A

Type II, III, and IV hypersensitivity reactions

110
Q

What is the autoantigen of autoimmune hemolytic anemia?

A

Rh blood group antigens

I antigen

111
Q

What is the consequence of autoimmune hemolytic anemia?

A

Destruction of red blood cells by complement and phagocytes

Anemia

112
Q

What is the autoantigen of graves’ disease?

A

Thyroid-stimulating hormone receptor

113
Q

What is the consequence of graves’ disease?

A

Hyperthyroidism

114
Q

What is the autoantigen of myasthenia gravis?

A

Acetylcholine receptor

115
Q

What is the consequence of myasthenia gravis?

A

Progressive weakness

116
Q

What is a type II hypersensitivity reaction?

A

Antibodies against cell surface receptors

117
Q

In type II hypersensitivity reactions, what does the antibody respond to?

A

Blood cell surface antigens

118
Q

In autoimmune hemolytic anemia, what do IgG antibodies against surface antigens trigger?

A

Cell destruction leading to anemia

119
Q

What is the autoantigen for systemic lupus erythematosus?

A 
DNA
Histones
Ribosomes
snRNP
scRNP
120
Q

What is a type III hypersensitivity reaction?

A

Formation of small immune complexes

121
Q

What is systemic lupus erythematosus?

A

Chronic IgG production against ubiquitous cellular antigens

122
Q

In systemic lupus erythematosus, what is a large amount of autoantigen produced by?

A

Apoptotic cells and damaged tissue

123
Q

In systemic lupus erythematosus, where are small immune complexes deposited?

A

In renal glomerulus

124
Q

In systemic lupus erythematosus, what causes inflammation?

A

Joints and blood vessels of the skin and other organs

125
Q

What are 5 examples of Type IV T cell mediated diseases?

A 
Type I diabetes
Rheumatoid arthritis
Multiple sclerosis
Crohn’s disease
Psoriasis
126
Q

What is multiple sclerosis?

A

T cell mediated response against myelin antigens resulting in destruction of myelin in the central nervous system

127
Q

What does multiple sclerosis result in?

A

Progressive muscle weakness
Blindness
Paralysis

128
Q

What is type I diabetes?

A

T cell mediated response against B cells in the pancreas resulting in insulin deficiency

129
Q

What does type I diabetes result in?

A

High blood sugar

130
Q

What is rheumatoid arthritis mediated by?

A

T cells and autoantibodies against antigens in the synovial membrane of joints

131
Q

What happens in rheumatoid arthritis?

A

Inflammation spreads to bone and cartilage

132
Q

What does rheumatoid arthritis result in?

A

Pain
Reduced function
Disability

133
Q

What is autoimmune disease thought to result from?

A

Genetic susceptibility, breakdown in tolerance mechanisms, and environmental triggers

134
Q

What does a relative risk of autoimmune disease greater than 1 indicate?

A

Increased susceptibility

135
Q

What does a relative risk of autoimmune disease less than 1 indicate?

A

Increased protection

136
Q

What do family studies of MHC genotypes in type I diabetes show?

A

Affected siblings inherit the same sets of MHC genes much more often than would be expected if MHC genotype did not influence susceptibility

137
Q

What modifies susceptibility to rheumatoid arthritis?

A

Genotype and environmental factors

138
Q

What do 4 of the DRB1*04 alleles do for rheumatoid arthritis?

A

Confer susceptibility

139
Q

What does the DRB1*04:02 allele do for rheumatoid arthritis?

A

Confers protection

140
Q

What does smoking do in individuals with the DRB1*04 susceptibility alleles do?

A

Increases susceptibility significantly

141
Q

In what gender do more autoimmune disease occur?

A

Female

142
Q

What are 4 examples of other genes that can predispose someone to autoimmunity?

A

Genes that affect autoantigen availability and clearance
Genes that affect apoptosis
Genes involved in signals that control lymphocyte activation
Genes that affect development or function of Tregs

143
Q

How can infections lead to an autoimmune disease?

A

By providing an inflammatory environment that promote lymphocyte activation

144
Q

What is molecular mimicry?

A

Antibodies produced against a pathogen epitope cross-react with self-peptides

145
Q

What is an examples of molecular mimcry?

A

Rheumatic fever

146
Q

Chapter 16 study guide and charts

A

Chapter 16 study guide and charts

147
Q

What is histocompatibility?

A

Donor and recipient have same antigens

148
Q

What are alloantigens?

A

Antigens that differ between members of the same species

149
Q

What are examples of alloantigens?

A

MHC molecules

ABO blood antigens

150
Q

What is an alloreaction?

A

An immune response against alloantigens

151
Q

What are alloreactions the major impediment to?

A

Successful transplantation

152
Q

What is an autograft?

A

Transplantation of a tissue from one site to another on the same individual

153
Q

Why can autograft be performed with 100% success?

A

Perfect histocompatibility because it is your own tissue

154
Q

What is an allograft?

A

Transplant of a tissue from one individual to another

155
Q

What is the most commonly transplanted tissue?

A

Blood

156
Q

In blood transfusions, what must the donor and recipient be matched for?

A

ABO and Rhesus D antigens

157
Q

Is MHC matching necessary for blood transfusions?

A

No

158
Q

What is the universal blood donor?

A

Type O Rh-

159
Q

What is the universal blood acceptor?

A

Type AB Rh+

160
Q

What is rejection of solid organ transplants due to?

A

An immune response to non-self MHC molecules

161
Q

In solid organ transplantations, what is a long-term outcome better with?

A

A high level of histocompatibility

162
Q

What is hyperacute rejection caused by?

A

Existing antibodies that react with antigens on endothelial cells in blood vessels of the grafted tissue

163
Q

What can existing antibodies that cause hyperacute rejection arise from?

A

Pregnancy
Blood transfusions
Previous transplants

164
Q

When does hyperacute reaction occur?

A

Within 24 hours of transplantation

165
Q

What happens to vessels in hyperacute rejection?

A

They become blocked and damaged leading to tissue death

166
Q

How can hyperacute reactions be avoided?

A

By blood typing and performing a cross match test

167
Q

What is acute rejection mediated by?

A

T cells recognizing the graft tissue as foreign

168
Q

What are transplants monitored for and treated with?

A

Symptoms of acute rejection episodes and treated with immunosuppression

169
Q

What is acute rejections a major risk factor of?

A

Chronic rejection

170
Q

What happens in indirect rejection?

A

Recipient APCs from the graft present processed antigens to recipient T cells on self MHC molecules

171
Q

In indirect recognition, what do recipient T cells recognize as foreign?

A

Donor MHC antigen fragments

172
Q

What happens in direct rejection?

A

Donor APCs from the graft present antigens to recipient T cells as MHC:antigen complexes

173
Q

What do receptor cells do in direct rejection?

A

Recognize the complex as foreign and direct effector cells against the foreign tissue

174
Q

What are minor histocompatibility antigens?

A

Alloantigens of non-MHC molecules

175
Q

What is chronic rejection caused by?

A

Chronic injury to the graft

176
Q

What are risk factors of chronic rejection? (3)

A

Acute rejection episodes
Pre-graft ischemia
Underlying disease

177
Q

What is graft versus hot disease?

A

The converse of acute allograft rejection

178
Q

What does graft versus hot disease result from?

A

Donor T cells attacking recipient tissues

179
Q

In hematopoietic stem cell procedure, why is the recipients bone marrow destroyed?

A

To reduce the number of recipients HSCs, immunosuppress the recipient, and reduce the number of tumor cells

180
Q

What does protocol of hematopoietic stem cell procedure do?

A

Damages dividing host cells

181
Q

What happens to donor hematopoietic stem cells?

A

They are infused and re-populate the recipients bone marrow

182
Q

What are sources of hematopoietic stem cells? (3)

A

Bone marrow
Peripheral blood
Umbilical cord blood

183
Q

What is hematopoietic stem cell transplantation used to do?

A

To treat various diseases

184
Q

What is mucopolysaccharidosis?

A

Various deficiencies of lysosomal enzymes

185
Q

What is Gaucher’s syndrome?

A

Deficiency of the lysosomal enzyme glucocerebrosidase

186
Q

What does acute graft versus hot disease primarily affect?

A

Skin, gut, and liver

187
Q

What do mature donor T cells do during graft versus hot disease?

A

Promote engraftment and reconstitute the recipient’s immune system

188
Q

What happens to immune reconstitution without mature donor T cells?

A

It is suppressed

189
Q

What is required for T cell function?

A

Some MHC histocompatibility

190
Q

What happens if the donor and recipient have different MHC alleles?

A

T cells that were positively selected by recipient MHC will not be able to become activated in the periphery by donor MHC

191
Q

In the correlation between hematopoietic stem cell transplantation outcome and MHC histocompatibility, how do you get the better outcome?

A

Fewer mismatches

192
Q

When do you not want fewer mismatches?

A

In graft versus leukemia

193
Q

How is allogenic hematopoietic stem cell transplantation usually performed?

A

Using an identical MHC matched sibiing or unrelated MHC matched donor

194
Q

What is the chance of an identical MHC match with a sibling?

A

25%

195
Q

Chapter 15 study guide and charts

A

Chapter 15 study guide and charts

196
Q

What do successful pathogens have to do?

A

Replicate in the host and be transmitted

197
Q

What must successful pathogens have?

A

Ways to evade the host immune system

198
Q

Are the most virulent pathogens the most successful?

A

Not necessarily

199
Q

What must successful hosts have?

A

An efficient immune response

200
Q

What are antibodies generated against one subtype like for other subtypes?

A

No effective against them

201
Q

What do different strains of a pathogen have?

A

Different surface antigens

202
Q

What do the influenza virus surface antigens have?

A

A high mutation rate

203
Q

Why are the surface antigens of influenza virus ever changing?

A

To evade recognition by the immune system

204
Q

What is antigenic shift?

A

2 or more different strains combine to form a new subtype

205
Q

What is antigenic drift?

A

Mutations occur slowly over time within a strain

206
Q

How can herpesvirus evade the immune system?

A

By persisting in a latent form

207
Q

What is herpesvirus normally controlled by?

A

The immune system

208
Q

What can herpesvirus cause when the immune system is compromised?

A

Recurrent infections

209
Q

What do herpes simplex virus and chicken pox virus persist in?

A

Neurons in latent form

210
Q

What does Epstein Barr virus persist in?

A

B-cells in latent form

211
Q

What does Cytomegalovirus persist in?

A

Lymphocytes, endothelial cells, and macrophages in latent form

212
Q

What are 4 different viral strategies?

A

Inhibition of humoral immunity
Inhibition of inflammatory response
Blocking of antigen processing and presentation
Immunosuppression of host

213
Q

What does S. aureus SSLP7 do to block the effector function of antibodies?

A

Binds to IgA Fc region and V5 to prevent both effector functionsAlso has a protein that binds Fc region of IgG

214
Q

What does HIV use as a receptor?

A

CD4

215
Q

What does HIV infect?

A

CD4 T cells macrophages and dendritic cell

216
Q

What does HIV replicate in?

A

Activated CD4T cells

217
Q

What does the outer glycoprotein of HIV have?

A

A high mutation rate

218
Q

What can HIV remain hidden from the immune system in?

A

Naïve T cells

219
Q

In HIV, what happens when T cells become critically low?

A

Patients become susceptible to infections normally well controlled by a healthy immune system

220
Q

Where does Mycobacterium tuberculosis replicate?

A

In macrophage endosomes

221
Q

Where does Plasmodium falciparum replicate?

A

In liver and RBCs which do not have low MHC class I expression

222
Q

What does Plasmodium falciparum produce?

A

Adhesion molecules in RBCs to prevent destruction

223
Q

What does Plasmodium falciparum secrete?

A

Cytokines that prevent a T memory response from developing

224
Q

What must happen in order for cancer to occur?

A

Tumor suppressor genes are tuned off

Oncogenes are turned on

225
Q

What is cancer caused by?

A

An accumulation of mutations that result in uncontrolled cell proliferation

226
Q

What happens in leukemia?

A

Malignant cells arise in the bone marrow and blood

227
Q

What are the 2 types of leukemia?

A

Myeloid and lymphoid

228
Q

What happens in lymphoma?

A

Malignant cells arise in the lymphatic system

229
Q

What happens in myeloma?

A

Malignant cells arise from plasma cells

230
Q

Does the immune system normally respond to tumor antigens?

A

Yes

231
Q

Are immunosuppressed individuals more or less prone to cancers that the general population?

A

More prone

232
Q

What are tumor associated antigens?

A

Antigens that are also found on normal cells, but at lower concentration

233
Q

What are tumor specific antigens?

A

Antigens that are not found on normal cells

234
Q

What are cancer/testes antigens?

A

Antigens commonly expressed in tumors that are normally only expressed in the testes and during fetal development

235
Q

What happens when successful tumors evade the immune system?

A

Down regulate MHC molecules

Tumor associated antigens are closely related to ‘self-antigens’

236
Q

What do successful tumors that evade the immune system secrete?

A

Anti-inflammatory cytokines that promote T cell tolerance

237
Q

What do successful tumors that evade the immune system produce?

A

Surface molecules that engage T cell receptors and cause anergy

238
Q

Chapter 17 study guide and charts

A

Chapter 17 study guide and charts

Immunology-Spring 2017 (4 decks)

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