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Immunology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Where do naive lymphocytes in the blood migrate to?

A

Secondary lymphoid tissues

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2
Q

Where do effector and memory T cells in the blood migrate to?

A

Site of infection

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3
Q

What are HEVs and what is their function?

A

High endothelial venules - specialized blood vessels which facilitate extravasation of lymphocytes into the lymph node

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4
Q

What are distinctive characteristics of HEVs (as compared to regular venules)?

A

Tall endothelial cells

Thick basal lamina

Concentrically arranged reticular fibroblasts making up a perivascular sheath

Increased expression of molecules associated with cell migration into lymphoid tissues

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5
Q

What are the four primary stages of lymphocyte trafficking from blood vessel to tissue, and which molecules facilitate them?

A

Rolling - Selectins
Activation - Chemokines
Adhesion - Integrins
Diapedesis - Chemokines

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6
Q

What are the three classes of molecules grouped as “adhesion molecules”?

A

Selectins, chemokines, integrins

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7
Q

What are chemokines and what is their function?

A

Small soluble (secreted) proteins. Chemoattractants for immune cells

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8
Q

What are selectins?

A

Cell surface proteins, allow for extravasation of immune cells

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9
Q

What are integrins?

A

Cell surface proteins, allow immune cells to migrate to specific tissues

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10
Q

What is monocyte-chemoattractant protein 1?

A

Mucosal homing receptor - Regulates migration and infiltration of monocytes/macrophages

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11
Q

What are the primary lymphoid organs?

A

Thymus, bone marrow/bursa fabricius, Ileal Peyer’s patch, lymphoglandular complexes

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12
Q

What are the (groupings of) secondary lymphoid organs?

A

Lymph nodes, spleen, tonsils, Peyer’s patches

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13
Q

Which part of the thymus is most densely packed with lymphocytes?

A

Cortex (outer part)

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14
Q

What is Hassal’s corpuscule?

A

Structure in the thymic medulla containing a blood vessel with very thick walls preventing antigen from entering the thymus.

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15
Q

What is the bursa fabricius and where is it located?

A

Primary lymphoid organ (source of B cells AND traps antigen) in birds. Round sac with a connecting duct to the cloaca

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16
Q

What are the two types of Peyer’s patches and what is the difference between them?

A

Ileal patch - site of lymphocyte (B cell) development

Jejunal patches - secondary lymphoid organ

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17
Q

What is the mammalian equivalent to the bursa fabricius?

A

Ileal peyer’s patch

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18
Q

Which animals do not have lymph nodes?

A

Birds

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19
Q

What are the residential cells of lymph nodes?

A

(Follicular) dendritic cells, follicular T helper cells

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20
Q

Which cells are located in the cortex vs. paracortex of the lymph nodes?

A

T cells in paracortex
B cells in cortex (follicles)

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21
Q

Where is the germinal center visible in the lymph node?

A

Round structure near the junction of cortex and paraxortex

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22
Q

Which B cell-related processes occur in the dark zone vs. light zone of the germinal center?

A

Dark zone - Somatic hypermutation
Light zone - Testing of antibody affinity

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23
Q

What is the primary cell type found in the subcapsular sinus of lymph nodes?

A

Macrophages

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24
Q

What are the three immune-related structures in tonsils/Peyer’s patches and which cell types are they associated with?

A

Dome region - macrophages and DCs
Follicles - B cells, follicular DCs/Th cells
Interfollicular region - T cells

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25
Q

What are the specialized cells associated with antigen uptake at mucosal surfaces (tonsils/Peyer’s patches)?

A

M cells

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26
Q

Which cells are highly prevalent in the marginal zone in the spleen?

A

APCs

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27
Q

Where are B and T cells located in the spleen?

A

B cells in follicles
T cells surrounding incoming arterioles

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28
Q

What is the largest immune compartment in the body?

A

Mucosal surfaces

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29
Q

What is the difference between inducive and effector sites in mucosal immunity?

A

Inducive sites are lymphoid tissues - where immune response is being induced (site of antigen uptake)
Effector sites are were we find mature lymphocytes that have been exposed to their specific antigen (e.g. lamina propria)

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30
Q

What are the specialized characteristics of M cells which allow them to transfer antigen to lymphocytes/APCs?

A

Shorter glycocalyx on apical side to create a physical trap for antigens/pathogens
Pockets on basal side where immune cells can access antigen

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31
Q

Other than M cells, what is another system by which immune cells can access antigen across mucosal surfaces?

A

DCs can extend their dendrites between epithelial cells to “fish” for antigen

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32
Q

In what tissue(s) are M cells located?

A

Epithelium of small intestine, colon, rectum, tonsils, and adenoids

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33
Q

What are the primary (immune) cell types found in the lamina propria of mucosal tissues?

A

B cells (mostly IgA, some IgG/IgE) and T helper cells (to provide a suitable microenvironment)

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34
Q

What are the primary (immune) cell types found in the intraepithelial tissue of mucosae?

A

Cytotoxic T cells

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35
Q

What is the mechanism by which IgA dimers cross mucosal surfaces to enter the epithelium?

A

Endocytosis/exocytosis by epithelial cells - facilitated by polyimmunoglobulin receptor (pIgR)

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36
Q

In what tissues do oral mucosal vaccines induce an effective immune response?

A

Small intestine, ascending colon, mammary and salivary glands

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37
Q

In what tissues do rectal mucosal vaccines induce an effective immune response?

A

Rectum only

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38
Q

In what tissues do nasal/tonsilar mucosal vaccines induce an effective immune response?

A

Upper airways, regional secretions, genital mucosa

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39
Q

In what tissues do vaginal mucosal vaccines induce an effective immune response?

A

Genital mucosa only

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40
Q

In what tissues do skin vaccines induce an effective immune response?

A

Possibly the gut. Ineffective in most mucosal surfaces

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41
Q

How is exclusion immunity induced?

A

If antigen is detected along with a danger signal either via M cells or DCs across the mucosa, an immune response will be induced and secretory antibodies will be produced

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42
Q

How is oral tolerance induced?

A

Non-adherent food antigens induce activation of Treg cells and suppression of Th1/Th2/Th17 inflammatory response

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43
Q

What are examples of cytokines produced by Treg cells in the case of oral tolerance of food antigens?

A

IL-10, TGF-b

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44
Q

What can cause oral tolerance of food antigens to fail?

A

When there is a large influx of food antigens past the GI mucosa due to increased permeability/damage to the epithelium

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45
Q

In terms of the immune system, what is the difference between commensal and pathogenic bacteria?

A

Location (if they cross/damage the epithelium, they are treated as pathogenic)

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46
Q

What are the six placental layers (in order) acting as the barrier between maternal and fetal blood? - assume epithelochorial placentation

A

Maternal endothelium
Endometrial CT
Uerine epithelium
Chorion epithelium
Fetal placental mesenchyme
Fetal endothelium

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47
Q

What are the three types of placentation (as it relates to proximity between maternal and fetal blood)?

A

Epitheliochorial (most layers)
Endotheliochorial
Hemochorial (fewest layers)

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48
Q

Which species have epitheliochorial placentation type?

A

Cows, pigs, horses

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49
Q

Which species have endotheliochorial placentation type?

A

Dogs and cats

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50
Q

Which species have hemochorial placentation type?

A

Humans and rodents

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51
Q

What is the importance of the thickness of the barrier between maternal and fetal blood?

A

Determines the extent to which maternal antibodies are able to enter the fetal bloodstream (thus determining the degree of reliance on colostrum for immunity)

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52
Q

Describe epitheliochorial placentation

A

Maternal side has both uterine epithelium and BV endothelium
No transfer of maternal antibodies

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53
Q

Describe endotheliochorial placentation?

A

Maternal side only has BV endothelium
Limited transfer of maternal antibodies

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54
Q

Describe hemochorial placentation?

A

Maternal side has neither uterine epithelium OR BV endothelium
Good transfer of maternal antibodies

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55
Q

Which type of immune response is suppressed during pregnancy?

A

Th1

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56
Q

What is the avian equivalent of IgG?

A

IgY

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57
Q

How is antibody transfer achieved in birds?

A

IgY is concentrated in the egg
IgM and IgA enter the albumin in the oviduct and are swallowed by the chick

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58
Q

From which point in gestation is the fetus able to mount an active immune response?

A

Second trimester

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59
Q

Which vaccine is routinely administered during fetal development and in which species?

A

Marek’s disease - chickens

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60
Q

What are the two primary reasons why a neonate is unable to mount an effective immune response against a pathogen?

A

Immune system is IMMATURE and IMPAIRED

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61
Q

What are the characteristics of the “neonate immune environment”

A
  • Th2 (mother) / Treg (neonate)-biased immune system
  • High levels of IL-10/Treg
  • High levels of corticosteroids after birth
  • Inability to mount effective IFN-g response
  • Passively transferred immunity
  • Developing mucosal immune system
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62
Q

Which hormone(s) are involved in immune suppression in neonates?

A

Corticosteroids

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63
Q

Which factor is primarily responsible for driving the maturation of the neonatal immune system?

A

Intestinal microbiota

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64
Q

What is the difference between passive and active neonatal immunity?

A

Passive = antibodies transferred from mother to offspring
Active = immune response of neonate to vaccination or infection

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65
Q

What is colostrum?

A

The first milk - essentially concentrated maternal serum, rich in maternal antibodies

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66
Q

What is the approximate time frame in which immunoglobulins from colostrum can be absorbed into the fetal circulation?

A

6-24hrs

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67
Q

What is a disadvantage to giving a neonate pre-purchased colostrum?

A

Colostrum from the mother contains antibodies (IgG) that are specific to the environment in which the mother (and therefore offspring) is living. Pre-purchased colostrum is not “personalized”

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68
Q

What is the contribution of milk to the immune system of offspring?

A

Contains antibodies from pathogens encountered in the maternal gut, thereby protecting the fetal gut

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69
Q

Other than immunoglobulins and immune cells, what are other crucial protein contents of colostrum?

A

Lactoferrin, lactoperoxidase, and lysozyme (nonspecific lysis/effects on growth of pathogens)
Insulin-like growth factor, epidermal growth factor, alpha lactalbumin, TGFb, IL1, CSF, IL6 (stimulates growth, cell division, protein synthesis, etc.)

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70
Q

Which immunoglobulin classes are more common in (non-ruminant) colostrum vs. milk?

A

Colostrum: IgG
Milk: IgA

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71
Q

How are the immunoglobulins secreted in milk produced?

A

Plasma cells migrate from the intestine to the mammary tissue via CCL28

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72
Q

Which problem is created by maternal antibodies in the neonate?

A

Immune interference - they can bind to and neutralize vaccines before the neonate can respond

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73
Q

What do IFNa and IFNb do?

A

Establish an anti-viral state (resistance to replication, increase ligands for NK receptors, activate NK cells)

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74
Q

What does IFNg do in the context of a Th1 response?

A

Activates (M1) macrophages, enhances CD8 T cell killing

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75
Q

What antibody class is produced during a Th1 response and what is its primary function?

A

IgG; primarily for virus neutralization and opsonization, as well as antigen-dependent cell-mediated cytotoxicity by NK cells

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76
Q

Which cells are targeted by HIV?

A

CD4+ T cells

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77
Q

What causes pigs infected with high-path strains of PRRSV to die?

A

Cytokine storm

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78
Q

How do bacteria interact with the complement system?

A

Motifs on bacterial cell surface can activate complement via alternative pathway. C3b can opsonize, C3a and C5a are anaphylatoxins, MAC forms

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79
Q

What are the roles of antibodies during bacterial infection/Th2 response?

A

Neutralizing toxins/bacterial attachment, opsonization, activating complement (classical)

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80
Q

What class of immune response is initiated by protozoa infection?

A

Th1/Th2

81
Q

What class of immune response is initiated by helminth infection?

A

Th2

82
Q

What class of immune response is initiated by arthropod parasites?

A

Th1/Th2

83
Q

What type of life cycle does toxoplasma have?

A

Extracellular pathogen with intracellular reproduction (Th1 response primarily)

84
Q

How have African trypanosomes evolved to evade the immune system?

A

Switching/shuffling of cell surface glycoprotein expression (evades antibodies)

85
Q

How do helminths evade the immune system?

A

Thick extracellular cuticle to prevent attachment of MAC, too big to phagocytose

86
Q

What is the body’s main response to helminth infection?

A

IgE antibodies (against salivary antigens) initiating mast cell and eosinophil degranulation, resulting in the worm detaching from the intestinal wall

87
Q

Against what arthropod proteins do our bodies primarily generate antibodies?

A

Salivary proteins

88
Q

How do arthropods evade our immune system?

A

Saliva has immune modulatory effect, suppressing inflammation

89
Q

What is the name for the immune response generated during the body’s second exposure to a pathogen?

A

Anamnestic response

90
Q

What is a DIVA vaccine?

A

One which allows us to Differentiate Infected from Vaccinated Animals

91
Q

What are some possible components of a vaccine (other than antigen/adjuvant)

A

Diluents, stabilizers, preservatives, etc.

92
Q

What is a multivalent vaccine?

A

One which contains multiple antigens

93
Q

What are the three main approaches to constructing a vaccine?

A

Whole (attenuated) pathogen, parts, or genetic material

94
Q

Describe the endogenous vs. exogenous pathways for antigen presentation

A

Endogenous: Intracellular pathogen breakdown, expression on MHCI
Exogenous: Extracellular pathogen phagocytosis and expression on MHCII

95
Q

What is cross-presentation of an antigen?

A

Exogenous antigen being processed via the endogenous pathway and expressed on MHCI

96
Q

What are the main advantages to using a live attenuated viral vaccine?

A

Very effective for intracellular pathogens, long-lasting rapid-onset immunity, strong antibody and T cell response (overall best response)

97
Q

What are the main disadvantages to using a live attenuated viral vaccine?

A

Shedding of vaccine virus into the environment, possible to revert to full virulence, not recommended if animal pregnant or immune compromised

98
Q

Which pathway(s) are activated by a live attenuated viral vaccine?

A

Endogenous and exogenous

99
Q

Which pathway(s) are activated by an inactivated viral or subunit vaccine?

A

Exogenous only

100
Q

What are the main disadvantages to using an inactivated viral vaccine?

A

Immune response not as strong, more short lived compared to live attenuated. Weak T cell response. Requires adjuvants

101
Q

What are the main advantages to using an inactivated viral vaccine?

A

Very safe (no reversion to virulence), no virus shedding

102
Q

What are the two types of subunit vaccines?

A

Split - purified from disrupted pathogen
Recombinant - expressed in other cells/virus then purified

103
Q

What are the main advantages to using a subunit vaccine?

A

Very safe, no shedding into the environment, very cost effective, strong antibody response

104
Q

What are the main disadvantages to using a subunit vaccine?

A

Immune response relatively weak and short-lived, weak T cell response, requires an adjuvant

105
Q

What is a vectored vaccine?

A

Desired target antigen is expressed on the surface of a non-pathogenic virus

106
Q

What are the main advantages to using a vectored vaccine?

A

Long-lasting and rapid immune response, strong antibody and T cell response, cannot revert to full virulence

107
Q

What are the main disadvantages to using a vectored vaccine?

A

Viral shedding into the environment, immunity against the vector can reduce efficacy of booster vaccines

108
Q

What are the main advantages to using a DNA/RNA vaccine?

A

Long-lasting and rapid-onset, good antibody and T cell response, no live pathogen involved

109
Q

What are the main disadvantages to using a DNA/RNA vaccine?

A

Delivery is complicated (requires a carrier or nanoparticles)

110
Q

What are replicons?

A

Self-amplifying RNA. Could potentially be utilized in vaccines

111
Q

What are common vaccine adjuvants (in inactivated or subunit vaccines)?

A

Aluminum, oil-in-water (squalene), etc.

112
Q

What are the three main functions of adjuvants?

A

Delivery of vaccine (depot effect, slow-release, localization)
Targeting of specific cells (APCs, specific tissues, etc.)
Stimulation of innate/acquired immune systems (danger signal)

113
Q

By what mechanism(s) can we create DIVA vaccines?

A

Typically involves removal of a marker protein from the vaccine. Animals which do not have antibodies against the marker have not been infected

114
Q

What is the main Canadian organization responsible for regulatory approval of vaccines?

A

CFIA Canadian Centre for Veterinary Biologics

115
Q

What are the primary players in a type I hypersensitivity response?

A

IgE, mast cells, basophils, and eosinophils

116
Q

What is the difference between an allergic reaction and anaphylaxis?

A

Allergy is local and not immediately life-threatening. Anaphylaxis is systemic and severe

117
Q

By what mechanism are tissues damaged during an allergic reaction?

A

Mast cell and basophil degranulation in response to antibody-bound IgE (contents cause vasodilation, pruritus, bronchoconstriction)

118
Q

At which sites is IgE mainly produced?

A

Body surfaces (skin, lung, intestine)

119
Q

What is the difference between “allergy” and “atopy”?

A

Allergy: Production of IgE in response to an antigen
Atopy: Production of IgE at abnormally high levels in response to many antigens

120
Q

What is FcERI and on which cell type(s) is it found?

A

Receptor with very high IgE binding affinity
Found primarily on mast cells and basophils, eosinophils to a lesser extent, and on DCs/monocytes of atopic patients

121
Q

What is FcERII and on which cell type(s) is it found?

A

Receptor with relatively weak IgE affinity
Found on NK cells, macrophages, DCs, eosinophils, platelets, and some B cells

122
Q

What is the function of histamine (released by mast cell degranulation)?

A

Smooth muscle contraction (bronchoconstriction), exocrine secretion of mucus, tears, saliva

123
Q

What is the function of serotonin (released by mast cell degranulation)?

A

Vasodilation/edema

124
Q

What is the function of arachidonic acid (released by mast cells)?

A

Precursor for eicosanoids, which in turn have effects on vessel tone and permeability

125
Q

What are the contents released during mast cell degranulation?

A

Histamine, serotonin, tryptase, Kallikreins, proteases, proteoglycans

126
Q

What cytokines are secreted by mast cells?

A

IL-4, IL-5, IL6, IL-13, TNF-a, MIP-1a

127
Q

Which cytokine activates eosinophils?

A

IL-5 causes mobilization and degranulation

128
Q

Which antibody receptor triggers eosinophil degranulation?

A

FcERII

129
Q

What are the two phases of a type I hypersensitivity reaction?

A

Sensitization: Phase of exposure which generates an IgE response
Re-exposure: Results in cross-linking of IgE on mast cells, triggering degranulation

130
Q

What are the primary clinical signs of anaphylaxis in sheep and cattle?

A

Dyspnea due to bronchoconstriction and pulmonary edema

131
Q

What are the primary clinical signs of anaphylaxis in horses?

A

Coughing, dyspnea, diarrhea

132
Q

What are the primary clinical signs of anaphylaxis in dogs?

A

Weakness and collapse

133
Q

What are the primary clinical signs of anaphylaxis in pigs?

A

Dyspnea

134
Q

What are the primary clinical signs of anaphylaxis in cats?

A

Dyspnea, scratching

135
Q

Where in the body do clinical signs of allergies typically manifest in dogs?

A

Skin (regardless of route of entry)

136
Q

What is urticaria?

A

Hives - acute local allergic response manifesting as wheals (lesions confined to the dermis)

137
Q

What is angioedema?

A

Generalized dermal edema which may progress to involve subcutaneous tissue

138
Q

Which cytokine plays a key role in atopic dermatitis and what does it do?

A

IL-31: Itch mediator and causes respiratory symptoms

139
Q

What is an a possible immune-related cause of food allergies?

A

IgA deficiency (failure of immune exclusion)

140
Q

How is hyposensitization accomplished in allergic patients?

A

Repeated subcutaneous injection of the allergen at increasing doses, promotes switching to a Th1 response (may require lifelong therapy)

141
Q

What is the basis of type II hypersensitivity?

A

Destruction of cells due to the binding of antibodies (IgG/IgM) to the cell surface - associated with NK cells, complement, and phagocytes

142
Q

What are the two primary means of RBC destruction in IMHA?

A

Phagocytosis in the spleen
Complement-mediated lysis in the bloodstream

143
Q

What are the five types of targets of antigen targets that could be associated with intra-vascular hemolysis?

A
  • Self RBC antigens
  • Alloantigens (blood transfusion)
  • Foreign antigens adsorbed to cell surface
  • Altered self antigen
  • Exposed cryptic antigen
144
Q

What is a major cross-match?

A

Mix recipient serum with donor cells

145
Q

What is a minor cross-match?

A

Mix donor serum with recipient cells

146
Q

What is HDN?

A

Hemolytic disease of the newborn - placental tears allow fetal blood to enter maternal circulation, mother mounts an immune response, antibodies concentrate in the colostrum, colostral antibodies cause hemolysis in the newborn

147
Q

What is the Direct Coombs Test for IMHA?

A

Can demonstrate antibodies bound to RBCs

148
Q

What is Evans Syndrome?

A

IMHA combined with immune mediated thrombocytopenia

149
Q

What is pemphigoid disease?

A

Type II hypersensitivity reaction - antibodies/complement targeting antigens in the epithelium. Lesions can be superficial to deep

150
Q

What is a potential cause of Addison’s disease?

A

Antibody-mediated targeting and killing of adrenal cortex cells

151
Q

What is a potential cause of diabetes mellitus?

A

Antibody-mediated targeting and killing of pancreatic beta cells

152
Q

What is myasthenia gravis?

A

Disease characterized by muscle weakness. Antibodies targeting Ach receptor, damaging the post-synaptic membrane

153
Q

What is the basis of type III hypersensitivity reactions?

A

Antigen-antibody complexes formed between soluble antigen in the serum or tissues

154
Q

What is the mechanism behind “immune complex disease”?

A

Type III hypersensitivity reaction occurs, forming immune complexes. Antibodies activate complement, including C3a and C5a, causing neutrophil and mast cell degranulation which damage tissues

155
Q

When are type III hypersensitivity reactions dangerous?

A

They are normal in small levels, but become dangerous when there is high levels of antigen and/or persistence of the antigen

156
Q

What is an “arthus reaction”?

A

Antigen injected subcutaneously into an animal with high levels of antibodies, resulting in neutrophil infiltration and inflammation within a few hours

157
Q

What is hypersensitivity pneumonitis?

A

Inhalation of antigen results in immune complex formation in alveolar walls (coughing/dyspnea)

158
Q

What is COPD?

A

Chronic obstructive pulmonary disease. Combination of type I and type III hypersensitivity reactions which occur in horses repeatedly fed mouldy hay

159
Q

How are serum immune complexes removed in generalized (intravascular) type III hypersensitivity reactions?

A

By binding to either RBCs or platelets which are removed by phagocytes

160
Q

What is the primary danger associated with generalized type III hypersensitivity reactions?

A

Large, insoluble immune complexes OR very large numbers of small soluble complexes can deposit in and block small blood vessels

161
Q

What is lupus erythematosus?

A

Antibodies to self antigens forming complexes in the basement membrane of the skin, kidney glomerulus, and small vessels

162
Q

How does rheumatoid arthritis occur?

A

Type III hypersensitivity reaction resulting in immune complex deposition in the synovial membrane

163
Q

What is the primary mechanism behind type IV hypersensitivity reactions?

A

Tissue damage due to activated macrophages and cytotoxic T cells. (Th1 response from antigen presented on APCs)

164
Q

What is the cause of a positive DTH test?

A

Inflammation occurs due to a population of memory Th1 cells in a previously exposed animal

165
Q

By what type of hypersensitivity reaction are granulomas formed?

A

Type IV - when antigen cannot be cleared. Remember that granulomas can contain multi-nucleate giant cells

166
Q

What is a potential pathological consequence to a persistent type IV hypersensitivity reaction?

A

Malabsorption syndrome due to granuloma formation in the gut

167
Q

What is leishmaniasis?

A

Granuloma formation resulting in granulomatous dermatitis caused by protozoa

168
Q

What is a cause of contact hypersensitivity?

A

Type IV hypersensitivity in response to prolonged exposure to small reactive molecules (latex, etc.)

169
Q

Describe the sensitization phase of contact hypersensitivity?

A

A molecule too small to be an antigen itself is absorbed into the skin and becomes associated with a “carrier” self-antigen, provoking an immune response

170
Q

What are the four types of grafts?

A

Autograft: within an individual
Isograft: between genetically identical individuals
Allograft: within a species
Xenograft: between species

171
Q

What is the main cause of allograft rejection?

A

Type IV hypersensitivity reaction to donor MHC or blood group antigens

172
Q

What is “graft versus host disease”?

A

Donor “passenger” lymphocytes reacting to (immunosuppresed) recipient tissue

173
Q

What is the “rheumatoid factor”?

A

Auto-antibodies to the Fc portion of IgG immune complexes (happen when antigen binding causes changes to Fc)

174
Q

What are cross-reactive antigens?

A

Pathogenic antigens which resemble self antigens (combines the common epitope with a danger signal)

175
Q

What is the cause of rheumatic fever?

A

Streptococcal cell walls causes cross-reactivity with host heart valve antigen

176
Q

What are the main differences between organ-specific and systemic autoimmune diseases?

A

Location, and organ-specific is more Th2, systemic is Th1 and Th2

177
Q

Which gene may be related to the development of systemic autoimmune diseases?

A

Deficiency in “aire”, an autoimmune regulatory gene which promotes self-antigen expression in the thymus

178
Q

What is combined immunodeficiency?

A

Failed development of lymphoid precursors

179
Q

What is thymic aplasia?

A

Failed development of T cells

180
Q

What is agammaglobulinemia?

A

Failed B cell development

181
Q

Where else can B cells fail?

A

Deficiencies in specific antibody classes

182
Q

What is the main immune deficiency seen in the innate immune system?

A

Neutrophil defects

183
Q

What is leukocyte adhesion deficiency?

A

Defect in adhesion proteins (CD18) which would allow neutrophils/T cells to leave the blood. Seen in Holstein cattle. Recurrent infection, fever, stunted growth, neutrophilia

184
Q

How long do SCID/agammaglobulinemia individuals typically survive?

A

As long as colostral Ig lasts (up to a few weeks)

185
Q

Which animals are known to have thymic aplasia?

A

Nude mice. No thymus

186
Q

What is the primary consequence of infectious bursal disease virus?

A

Damage to bursa fabricius leading to impaired B cell development. More severe in young birds

187
Q

What is the main difference between FIV and HIV?

A

HIV targets CD4 T cells specifically. FIV targets all T cell types

188
Q

How does canine distemper affect the immune system?

A

Infects and destroys secondary lymphoid tissues, depresses lymphocyte and macrophage activity

189
Q

How do viruses like feline panleukopenia, canine parvovirus, and african swine fever affect the immune system?

A

Destroy all rapidly dividing cells, including those in germinal centers

190
Q

What is the main gene involved in tumor suppression that, when mutated, causes cancer?

A

p53

191
Q

What are the two phases of tumor growth?

A

Avascular phase (tumor is dormant)
Vascular phase (rapid growth and angiogenic switch)

192
Q

Which cytokines promote an immune suppressed state in tumors?

A

IL-10 and TGFb

193
Q

Which cell surface protein on tumors inhibits Teff cells?

A

PDL1

194
Q

What are the three types of cell surface antigens that are abnormal in tumors?

A

Reactivated gene products (developmental genes), viral antigens, and mutated gene products

195
Q

What are MICA and MICB?

A

Stress molecules recognized by NK cells

196
Q

What are the two main mechanisms by which we can use immunotherapy to induce an effector state against tumors?

A
  • Overcoming the suppression in the tumor microenvironment
  • Immunizing against a specific antigen
197
Q

What are dendritic cell vaccines?

A

Patient DCs are isolated and exposed to the antigen of interest in vitro, then inject them back into the patient to induce a cell-mediated response

198
Q

How can monoclonal antibodies be used in cancer therapy?

A
  • Complement cytotoxicity
  • Antibody coupling to a toxin, cytokine, radioisotope
  • Targeted chemo (antibody coupled to an enzyme which activates a cytotoxic drug)
  • Antibody-induced apoptosis
199
Q

How are cytokines used in cancer therapy?

A

Dangerous to administer systemically (capillary leak syndrome, rash, fever, chills, nausea, depression) but can be injected directly into a tumor

Immunology (2 decks)

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