Immunology Flashcards

1
Q

What are the three branches of immune response?

A

Innate, intrinsic, adaptive

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2
Q

What is unique about adaptive immunity?

A

Provides memory and specificity

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3
Q

What is superoxide?

A

O2-, incredibly reactive, destroys lipid

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4
Q

What does superoxide dismutase do?

A

Turns reactive material into water

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5
Q

Is respiratory burst an oxygen-dependent action?

A

Yes

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6
Q

What types of cells/materials carry out oxygen-independent killing?

A

Low molecular weight defensins, cathepsin G, lysozyme, lactoferrin, proteolytic and/or hydrolytic enzymes

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7
Q

What is the purpose of C3B in the complement cascade?

A

Binds to invader so the system can “see” it

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8
Q

What is the purpose of C3A in the complement cascade?

A

Promotes inflammation

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9
Q

What is DAF and what does it do?

A

Decay accelerating factor, prevents continuation of complement cascade (Useful in transplantation)

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10
Q

What does antigen presentation cause the expansion of?

A

B cells producing antigen-specific antibody, and cytotoxic T cells that can lyse infected cells

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11
Q

How is specificity brought to the immune system?

A

Through antibodies

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12
Q

How does the time for IgM and IgG responses differ between an initial infection and a secondary infection?

A

IgM quick to respond in first infection as IgG creates specific antibodies, in second infection IgG is first to respond with cells that remember the initial infection

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13
Q

Why is TRIM5alpha special to intrinsic immunity?

A

Resistant to HIV, recognizes all viruses in a family and destroys the virus as soon as it enters a cell

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14
Q

What parts of an immunoglobulin make up the antigen binding site?

A

Light and heavy chains

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15
Q

Why is a constant domain important in an immunoglobulin?

A

So that the body can recognize it as “self”

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16
Q

In terms of an immunoglobulin, what do V, D, and J stand for?

A

Variable region, diversity, joint region

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17
Q

How are the heavy and light chains connected to each other?

A

Disulfide bonds

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18
Q

What do the FAB region and Fc region stand for?

A

Fragment antigen binding, Fragment crystallizable or Fragment constant

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19
Q

What are the three types of antibody variation?

A

Idiotypic (Change in antigen-binding site), allotypic (Change in AA sequence of heavy or light chain, inherited), isotypic (Change in light/heavy chain classification)

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20
Q

What are the possible types of light chains in antibodies?

A

Kappa or lambda

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21
Q

What are the possible types of heavy chains in antibodies?

A

Mu, Alpha, Delta, Gamma, Epsilon

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22
Q

What is the name of the site where antigens bind to anibodies, and which type of of site is more effective (Linear or conformational)?

A

Epitope, conformational (Normally live attenuated vaccines)

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23
Q

Name some features of IgG.

A

Secondary response to antigen, binds Fc region, neutralizes antigen and fixes complement (Signals for phagocytosis), high affinity due to affinity maturation

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24
Q

What three antibodies are transferred to offspring through colostrum?

A

IgG (Most), IgA (Intermediate), and IgM (Least)

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25
Q

Name some features of IgM.

A

Most primitive antibody, first responder to invasion, pentameric, low affinity but high avidity, neutralizes antigen and fixes complement

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26
Q

Name some features of IgA.

A

Most abundant in the body, can be dimeric or trimeric, heavy glycosylated hinge region, found in mucosal epithelium, has a secretory component, must be able to resist proteolytic degradation

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27
Q

Name some features of IgE.

A

Triggers histamine release (Regulate allergic responses) and mast cell degranulation, are present on the surface of mast cells, coats parasites and causes basophils/eosinophils to burst on parasite

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28
Q

Name some features of IgY.

A

Found in water birds (And a few other species), descendant of IgG and IgE, has no Fc region (Thought to cut down on allergies)

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29
Q

How does IgG differ in camelids?

A

Many only have a heavy chain which helps the molecule fit in tighter areas

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30
Q

Where do antibodies originate from?

A

B cells

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31
Q

Name some stages in the development of the plasma cell.

A

Hematopoietic stem cell, lymphoblast, lymphocyte, plasma cell

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32
Q

How are B cells selected for a specific antigen?

A

We make B cells against all known antigens, choose the one that works for a specific antigen, and get rid of the rest

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33
Q

What do plasma cells do?

A

Produce protein/antibodies (Have ER for protein production)

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34
Q

What is the fate of most virgin B cells?

A

Apoptosis in over 75%

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35
Q

Where does B cell variable region rearrangement occur to give rise to specificity?

A

Bone marrow

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36
Q

Once DNA is arranged, how is an antibody changed to improve affinity (NOT specificity)?

A

Can only be changed through the heavy chain

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37
Q

Name some features of class (Isotype) switching of antibodies.

A

Cannot switch back once a switch has occurred (Can go from IgM to IgG but not IgG to IgM), variable region sits right in front of the expressed class, when switching occurs the regions for other classes are excised away, occur in lymph follicles

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38
Q

How does IgM aid the production of IgG?

A

IgM provides time for the body to produce IgG

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39
Q

How do B cells react to a primary exposure to an antigen?

A

Produce plasma cells for antibody production and also start a B cell memory pool

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40
Q

How do booster work?

A

Given after the first vaccine has given the body enough time to weed out unsuitable B cells

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41
Q

How do B cells react to a secondary exposure to an antigen?

A

Call more memory cells and plasma cells to the area very quickly and in high amounts

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42
Q

What cells can be antigen presenting cells?

A

Macrophages, follicular dendritic cells, and B cells

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43
Q

Name some characteristics of clonal immune response.

A

Germline, same DNA in all cells from the line, labs measure DNA rearrangement, can be dangerous

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44
Q

Name some characteristics of polyclonal immune response.

A

Reactive, non-malignant, from a wide range of DNA

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45
Q

How do B cells get in and leave the lymph node?

A

Come in through blood vessel, circulate out through efferent pathway

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46
Q

What is lymphocyte trafficking?

A

Directing lymphocytes to different parts of the body using homing signals (To the lymph nodes or to a target tissue)

47
Q

What is somatic hypermutation?

A

How the immune system adapts to challenges, affinity maturation

48
Q

What is the life expectancy of a B cell if it fails at every stage?

A

If it fails to access target tissues: 2-3 days
If it fails to encounter an antigen: Half life is 3-8 weeks
Plasma cells can last possibly years

49
Q

When does a B cell become anergic (Unresponsive to antigens)?

A

When it reacts to a self antigen

50
Q

Where do T cells mature?

A

In the thymus (NOT THYROID)

51
Q

What needs to be present in order for an immune reaction to occur?

A

B cell, T cell, antigen presenting cell, antigen, antibody

52
Q

After what stage does the thymus begin to atrophy?

A

After puberty

53
Q

What happens if there is no thymus?

A

T cells are not produced and therefore immune reactions do not occur

54
Q

When is a T cell positively selected?

A

When it appropriately interacts with MHC Classes I and II on an cortical epithelium

55
Q

When is a T cell negatively selected?

A

When it inappropriately interacts with MHC Classes I and II and a self-peptide

56
Q

In what situations is MHC Class II present?

A

With Helper T cells and with CD4 for stabilization (Has alpha and beta chains)

57
Q

In what situations is MHC Class I present?

A

With cytotoxic T cells and with CD8 for stabilization (Only has alpha chain)

58
Q

Do thymocytes express CD4 or CD8?

A

Both

59
Q

What two things can the T cell do once it enters the thymus?

A

It can expand or can create a germinal center with B cells

60
Q

What interactions do T cells participate in when they are in lymph nodes?

A

Interact with dendritic cells to become primed, help B cell expansion

61
Q

How does the presence of an antigen lead to the creation of a germinal center?

A

Antigens are taken up by an antigen presenting cell, which breaks up the antigen and presents it to a helper T cell via MCH Class II. The helper T cell then releases cytokines to call B cells to the area, they both expand and create a germinal center

62
Q

Name three responses of Th1 (T helper).

A

Stimulate proliferation of Tc (Cytotoxic T) cells, increase macrophage activity, and help B cells produce antibody

63
Q

Name three responses of Th2 (T helper).

A

B cell proliferation, class switching, increase IgG production (Provides signal for a large organism such as a worm to be covered in antibody and then be covered in granules, favor humoral response and induce mast cell production)

64
Q

What does Th17 do?

A

Produces cytokines that promote neutrophil response, which are good at fighting fungi

65
Q

What keeps T cells from becoming inappropriately active?

A

The vast amount of interactions that must take place simultaneously between a T cell and a legitimate antigen-presenting cell in the presence of an antigen.

66
Q

How does an infected cell signal to the body that it is infected?

A

A part of the antigen is presented on MHC Class I that is required on all cells (In case apoptosis is needed) and it is recognized by a cytotoxic T cell, which releases cytokines and granules onto the infected cell

67
Q

How do NK cells kill virus-ridden cells?

A

ADCC, Antibody dependent cytotoxic toxicity

68
Q

How are exogenous antigens processed for presenting?

A

Endocytosed into antigen-presenting cell, proteolyzed into small peptides, combine with MHC Class II from Golgi and move to the surface to present to T cell

69
Q

How are endogenous antigens processed for presenting?

A

Move through proteosome to become small peptides, peptides move into Golgi, combine with MHC Class I INSIDE Golgi, move to cellular surface to present to T cell

70
Q

What types of antigens bind to MHC Class II?

A

Exogenous antigens

71
Q

What types of antigens bind to MHC Class I?

A

Endogenous antigens

72
Q

Why is MHC non-specific?

A

It recognizes different anchoring residues between individuals, can adapt to a wide range of pathogens

73
Q

Name some disadvantages of killed vaccines.

A

Hazardous to personnel handling it, hazardous to livestock if released into environment, must make sure it is completely inactivated, cellular components may cause side effects, normally requires more than one treatment, cold chain required for storage/transport

74
Q

Name some disadvantages of live attenuated vaccines.

A

Cold chain required for storage/transport, some residues from medium used for growth, short shelf-life, possible reversion to virulent form

75
Q

Name some adjuvents.

A

Freud’s Incomplete, Freud’s Complete (No longer allowed in vet med due to granuloma occurrance), Alum, ISCOMS (Immune stimulating complexes)

76
Q

What phenomenon can allow dizygotic twin calves to accept skin grafts/organ transplants from one another without adverse effects?

A

Tolerance, when placental fusion occurs and exchange hematopoietic stem cells, thereby becoming able to tolerate each others’ MHCs

77
Q

What are some examples of organ-specific autoimmune disorders?

A

Canine hypothyroidism, insulin-dependent diabetes mellitus (IDDM), Addison’s Disease, Hashimoto’s disease, and Grave’s disease

78
Q

Name some examples of non-organ-specific autoimmune disorders.

A

Rheumatoid arthritis, myasthenia gravis, pemphigus foliaceus, immune-mediated/autoimmune-mediated hemolytic anemia

79
Q

How are severe AITP and AIHA treated?

A

Oral corticosteroids, min. 4 weeks for AIHA, 1-2 weeks max for AITP

80
Q

How are chronic AITP and AIHA treated?

A

Cytotoxic drugs then corticosteroid or cyclosporin, treated for 4-5 months, given every day, then every other day, then tapering dose

81
Q

Which type of allergy is characterized by the binding of antigen to surface IgE, causing degranulation of mast cells and release of inflammatory agents?

A

Type I

82
Q

Which type of allergy is characterized by the binding of antibodies to surface components of cells, altering their antigenicity causing B cells to destroy the cell?

A

Type II

83
Q

Which type of allergy is characterized by the binding of soluble protein antigens to immunoglobulins, creating an immune complex which sticks to vessel walls and activates the complement cascade?

A

Type III

84
Q

Which type of allergy is characterized by antigenic-specific effector T cells?

A

Type IV

85
Q

How are the granule contents of a mast cell released in Type I hypersensitivity?

A

Histamines released first, then steroid, then adrenaline

86
Q

What do histamines do?

A

Increase permeability of vessels to let leukocytes attack the foreign matter

87
Q

What type of reaction are sweet itch and heaves?

A

Type I

88
Q

What main antibody is involved with Type II hypersensitivity?

A

IgG

89
Q

What are the results of Type II hypersensitivity?

A

Hemolytic anemia, autoimmunity

90
Q

What are the results of Type I hypersensitivity?

A

Asthma, anaphylaxis

91
Q

Neonatal isoerythrolysis is an example of which type of hypersensitivity?

A

Type II

92
Q

How does an immune-complex cause a hypersensitivity reaction?

A

Because the complex is too large to be phagocytosed, so basophils are called to the area and degranulate on the complex which causes vasodilation. The complex becomes stuck in the vessel and activates complement again, which calls more basophils to the area, and the process repeats

93
Q

What are the results of Type III hypersensitivity?

A

Farmer’s lung, Arthus reaction (Tetanus vaccine), serum sickness

94
Q

How does a Type IV hypersensitivity occur?

A

A helper T cell binds to an “antigen” and cytokines are released to produce more Th1 cells, which release more cytokines. Th2 cells are then activated which destroy cells on contact, and macrophages produce hydrolytic enzymes.

95
Q

What are the results of a Type IV hypersensitivity?

A

Chronic asthma, contact dermatitis, tuberculin reaction

96
Q

What is hyposensitization?

A

Using low to increasing levels of antigen to switch the immune reaction from IgE to IgG to prevent a hypersensitive reaction

97
Q

What would an animal be susceptible to if it had an IgA deficiency?

A

Upper respiratory tract infections because IgA protects mucus membranes

98
Q

What is LAD?

A

Leukocyte Adhesion Deficiency, prevents leukocytes from migrating into tissues at areas of inflammation

99
Q

What is the point of hemagglutinin and neuraminidase?

A

Hemagglutinin allows influenza virus to bind to molecules with sialic acid on glycoproteins of host cells, then neuraminidase allows the virus to exit the cell once it has used the host cell

100
Q

What is the difference between antigenic drift and antigenic shift?

A

Antigenic drift is when a virus mutates and antibodies have a lower affinity for the new mutation. Antigenic shift is when two or more strains of a virus combine to form a new strain with a combination of surface antigens

101
Q

How are viruses-infected cells killed?

A

With cytotoxic T cells

102
Q

How are viruses non-specifically inhibited?

A

Interferons create a hostile environment surrounding the infected cell, inhibit replication and release of viral particles, up-regulate MHC, stimulate NK and Th cells

103
Q

What are the three functions of NK cells?

A

Produce cytokines, lyse infected cells, and kill cells by ADCC (Antibody-dependent cellular cytotoxicity)

104
Q

How can viruses hide from the immune system?

A

Can become latent within the system until reactivation occurs or can integrate with host DNA to be latent

105
Q

How do ELISA tests work?

A

A well is coated with antibody specific to the testing antigen. The substance being tested is added and allowed to bind, then is washed away. Then another antibody-enzyme conjugate is added to bind to the antigen, if it is present, and then washed away. Then a chromogenic substrate is added, and the results are related to the amount of color present. (Positive = color, negative = no color)

106
Q

How is an ELISA performed for antibodies?

A

A well is coated with antigen, then the testing antibodies are added and allowed to bind, then washed away. Another antibody-enzyme conjugate is added to bind to the antibody, then washed away. A chromogenic substrate is added, and the resulting absorbance is read with a microplate reader

107
Q

How is progesterone tested in an immunoassay?

A

Progesterone added to wells with antibodies, washed away, progesterone-enzyme complex added, washed away, chromogenic substrate added, amount of color inversely related to amount of progesterone (Little color = +++Progesterone, +++Color = Little progesterone)

108
Q

How do immunodiffusion/precipitin tests work?

A

Put patient’s antibodies in agar in a test tube, add solution of supposed antibody, allow diffusion to occur, presence of a precipitin ring shows binding between antibody/antigen

109
Q

How do erythrocyte agglutination tests for felines work?

A

Have two wells, one with anti-B antiserum, one with anti-A antiserum. Add blood to both wells, the blood type is the well that agglutinizes

110
Q

How is immunofluorescence used to detect the presence of an antigen?

A

Primary antibody added to tissue, then antibody-antibody with fluorescent tag is added, use UV microscope to detect presence of binding

111
Q

What is flow cytometry?

A

Dripping solution in front of a laser and reading the refractory beams for size and granularity

112
Q

How do rapid immunomigration tests work?

A

Solution with possible antigen is added to the well. If antigen is present, it will bind to marked antibodies in the well. It then travels up the wick, and if antigen is present, it will be picked up by a second antibody in the test reading area.

113
Q

How are neutralizing antibodies tested for?

A

Dilutions of serum placed in wells, then antigen is added and the plate is incubated. Then the solution is put on indicator cells and incubated for 5 days. Positive presence of neutralizing antibodies is 75% of plaque reduction