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First Year Veterinary School > Immunology- Exam # 3 > Flashcards

Immunology- Exam # 3 Flashcards

1
Q

What is an important co-stimulatory molecule in signal transducing?

A

CD79

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2
Q

What is CD79 made of?

A

Alpha and Beta chains

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3
Q

TRUE of FALSE: B cells are always CD79 negative

A

FALSE- B cells are always positive for CD79.

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4
Q

How many CD 79’s are located next to the heavy chain?

A

2 one on each side.

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5
Q

TRUE or FALSE All T Cells are CD3 positive

A

TRUE

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6
Q

For B lymphocytes, what are other important co-stimulatory molecules? What do they do?

A

CD 21- Complement receptor for C3 (Binds to C3d)
CD 19- Signaling component (Binds to CD21)

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7
Q

TRUE or FALSE: Antigen does not have to be attached to the B Cell Receptor for their to be interaction with CD21 and CD 19

A

FALSE: The antigen MUST be attached.

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8
Q

What are the two major pathways leading to formation of NF-kB and NF-AT?

A

Phosophorolation of proteins —-> which activates transcription factor NF-KB
High levels of calcium —> which activate transcription factor NF-AT.

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9
Q

What can these transcription factors cause to happen after gene transcription?

A

Division
Apoptosis
Immunoglobulin Synthesis
Switching of Immunoglobulin manufacturing.

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10
Q

What is the functions of IL- 4?

A
  • Stimulates B cell growth and differentiation
  • Activates Mast Cells
  • Increase expression of MHC II - Induces Ig Class switching
    • IL-5 and IL-4 induced IgE production
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11
Q

What is the functions of IL- 5?

A
  • Stimulates B cell growth.
  • Mobilizes and activates eosinophils.
  • Stimulates IgM and IgG production
  • IL-5 and IL-4 induced IgE production
  • Selectively stimulates IgA production
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12
Q

What is the functions of IL- 13?

A
  • Stimulates B cell growth. - Suppresses macrophage functions
  • Similar to IL-4
  • Required for optimal induction of IgE
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13
Q

What is the functions of IL-9

A

T cell growth factor

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14
Q

What is the functions of IL-10

A
  • Inhibits Th1 cell function
  • Suppresses macrophage function.
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15
Q

What other factors are inhibited by IL-4 and IL-10?

A

IL-2 and IFN-gamma
Overall TH1 cells

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16
Q

What cell and cytokines promote the Humoral Immune Response?

A

TH2 cells
- IL-4 , IL-5, IL-9, IL-10, IL-13

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17
Q

What does all APC have?

A

CD40

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18
Q

In primary response, TH2 cell emits IL-4, IL-13, and IL-5. This will cause B cell to undergo?

A

Activation and division of B cells.

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19
Q

After activation and division which cytokine leads to differentiation?

A

IL-6

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20
Q

Why types of cells are differentiated from B cells?

A
  • Plasma cells (produce antibodies)
  • Memory Cells.
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21
Q

In the secondary response Memory cells work as?

A

Antigen Presenting cells.

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22
Q

What is the out come of the secondary immune response?

A
  • More plasma cells
  • More memory cells
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23
Q

What is some functions of IL-6?

A
  • Needed for final differentiation of B cell into plasma cells.
  • IL-6 + IL5 promotes IgA production
  • IL-6 + IL-1 promotes IgM production
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24
Q

The CD40 cell that is located on the B-cell will interact with what molecule on the T cell?

A

CD-154

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25
Q

The CD86 molecule on the B cell will interact with what molecule on the TH2 cell?

A

CD28

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26
Q

TRUE or FALSE: During a secondary immune response, the B cell itself can act as an antigen presenting cell

A

TRUE

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27
Q

CD40 and CD154 participate in a dialogue between T cells and professional APCs, what is the result of this interaction?

A

Both cell types are stimulated.

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28
Q

T cell stimulation has what affect on B cells?

A

T cell stimulation permits B cell proliferation and immunoglobulin production.

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29
Q

What Cells have CD40?

A

Professional antigen presenting cells such as: B-cells, Dendritic cells, and Macrophages.

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30
Q

Dendritic cells have what roles?

A

Antigen presentation
Cytokine production
Cell survival

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31
Q

Macrophages have what role?

A

Cytokine production/ activation
Phagocytosis

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32
Q

Of Dendritic cells, B cells, and macrophages, which cell type can trigger a brand new adaptive immune response?

A

Dendritic Cells

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33
Q

If antibody requires interaction with T helper cells they are called?

A

T dependent immune response

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34
Q

When receiving multiple doses of vaccines, what is the antibody you would see affected in the first vaccine ? Which in the second? Is the response the same each time? What if a 3rd response is introduced? What kind of immune response will you see this in?

A

Primary immune response (1st dose) triggers IgM
Secondary immune response (second dose) triggers IgG.
Each time the response increases due to memory.
The third dose would trigger an even stronger immune response.
You will see this in a T dependent immune response

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35
Q

If an antibody does not require interaction with a T cell, what is it called? What antibody will you see after the first dose? After the second dose?
Why is that?

A 
T- independent immune response. 
1st dose - IgM 
2nd dose- IgM 
No participation of Helper T cells, Only IgM response, No memory cells, No immunoglobulins class switching.
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36
Q

TRUE or FALSE: B cell receptors can only bind to processed antigens.

A

FALSE: B cell receptors can bind to FREE SOLUABLE antigens. B Cells recognize native epitopes.

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37
Q

What is the process of B cell production and where is each step occurring?

A

Stem Cell (Bone Marrow) –> Pre B cell (Bursa, Bone Marrow, Peyers Patches) –> Immature B cell (Bone Marrow, Bursa, Peyers Patches) –> Mature B Cell (Lymph nodes, Spleen, Bone Marrow) ( Antigen interaction will cause the mature B cells) –> Plasma cell (Lymph nodes, Spleen, Bone Marrow) –> This will cause immunoglobulin secretion

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38
Q

Where does the adaptive immune response begin
?

A

Secondary lymphoid organs

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39
Q

Immature B cells already have what kind of receptors?

A

IgM and IgD

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40
Q

What can mature B cells do?

A

increase IgM B cell receptors, increase MHC II, increase production of IL-4, IL-5, IL6, TNF-alpha, TGF- Beta.

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41
Q

How many antibodies can plasma cells can be produced per second?

A

10,000

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42
Q

What molecules cause class switching and what do they switch to?

A

IL-4 ——> IgG, IgE
IFN-gamma ——–> IgG
TGF- Beta ———> IgA
IL-5, IL-6 ——-> IgG, IgM, IgA

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43
Q

What are characteristics of plasma cells?

A
  • Typically Short lived 1-2 weeks, residing in spleen and lymph nodes after immunization.
  • There are also long lived population, which lives for months- years and accumulate in bone marrow.
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44
Q

What are characteristics of memory cells?

A
  • Long-lived resting memory cells, survival does not depend on antigen contact.
  • Large and dividing memory cells. Survival depends on antigen contact.
    Example: Memory cells survive 60 years in humans.
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45
Q

What specific location does this immune responses take place in the secondary lymphoid organs?

A

Germinal Centers ( Stimulated B cells and Th cells migrate to germinal center around 6 days after response begins)

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46
Q

What are the immunoglobulin classes?

A

IgG, IgM, IgA, IgE, IgD

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47
Q

Where can you find antibodies in the body?

A

Bodily fluids, Blood, Serum

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48
Q

What does antibodies fight against?

A

Virus
Protozoa
Bacteria
Toxins

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49
Q

List the types of immunoglobulins by highest to lowest serum concentration.

A
  • IgG
  • IgM
  • IgA*
  • IgD
  • IgE
    * IgA is in higher concentration in the saliva milk and gastrointestinal fluids.
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50
Q

What immunoglobulins are synthesized in the respiratory tract and intestinal tract?

A

IgE and IgA

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51
Q

What immunoglobulins are synthesized in the spleen and lymph nodes?

A

IgM, IgG, IgD

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52
Q

What Immunoglobulin class has the highest number of subunits?

A

IgM

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53
Q

What are the three types of globulins and where is the immunoglobulins located?

A

Alpha, Beta, and Gamma.
Immunoglobulins are located in the Gamma.
IgM is the only one that is located in the beta area.

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54
Q

What are the 2 common light chains?

A

Gamma and Lamda

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55
Q

IgG characteristics

A

Plasma cells located in spleen, lymph nodes, and bone marrow.

  • Important in inflammation.
  • Agglutination ( antibodies coming together)
  • Opsonization
  • Activate the classical complement pathway
  • 2 antigen binding sites
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56
Q

IgM characteristics

A

Plasma cells located in secondary lymphoid organs.

  • Acting as BCR (IgM is an Ig Monomer)
  • Complement activation site is Ch4 ( lowest area of the heavy chain)
  • Major Ig produced in primary immune response
  • Opsonization
  • Virus Neutralization
  • Agglutination
  • Not very important in inflammation.
  • 10 sites to bind antigen
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57
Q

IgA characteristics

A

Secretory IgA present on bottom.

  • Plasma cells in body surfaces: Intestines, Respiratory tract, urinary system, skin, and mammary gland.
  • Transported through interstitial epithelial cells int external secretions.
  • Major Ig in the external secretions of non ruminants.
  • IgA does not activate the classical complement pathway
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58
Q

IgG characteristics

A
  • Produced by plasma cells located under body surfaces.
  • IgE is attached to FcERI on mast cells and basophils.
  • IgE + antigen —–> inflammation.
  • Releases inflammatory molecules from mast cells.
  • Inflammation enhances local defense.
  • Immunity against parasites.
  • Shortest half life of all Ig’s
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59
Q

IgD characteristics

A

* intersting that mice have a larger hinge region then other mammals*
* No disulfide bond so the IgD is highly unstable.
- Not present in cats, chickens, and rabbits.
- IgD is mainly attached to B cells
- Some circulating IgD binds to basophils ( Basophils can then produce IL-4, IL-1 , canthelicidins, and B cell activator factor)
- Mediates the link between innate and adaptive immune response.

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60
Q

What are Isotypes?

A

Isotype antigenic determinants characterize the classes and subclasses of heavy chain and types and subtypes of light chains. More like specific to.a species as a whole

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61
Q

What is allotypes?

A

Allotype antigenic determinants are specified by the allelic forms of the Ig genes. More like a multiple individuals will have similar but will be different from other individuals.

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62
Q

what are idiotypes?

A

Idiotypes are the unique antigenic determinants present on variable heavy chain and variable light region of individual antibody molecules. More like specific to an individual

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63
Q

What three genes code for the variable domain?

A 
V= variable gene 
D= diversity gene 
J= joining gene
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64
Q

What immunoglobulin class is not present in felines?

A

IgD

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65
Q

What class of immunoglobulin activates the classical pathway of complement activation?

A

IgG and IgM

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66
Q

What class of immunoglobulin activates the lectin pathways of complement activation?

A

IgA

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67
Q

Which subclass if IgG is the best at activating the classical pathway of complement activation?

A

IgG3

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68
Q

Which class of immunoglobulin can be passed through the placenta? Which of its subclasses is best suited to do so?

A

IgG. IgG1 is the best suited

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69
Q

Which class of immunoglobulin has high affinity binding to mast cells and basophils?

A

IgE

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70
Q

What class of immunoglobulin creates systemic protection?

A

IgG

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71
Q

What kind of antibody provides immunity in mucosas?

A

IgA

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72
Q

Where can we find IgE antibodies?

A

Skin, mucus

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73
Q

What antibodies are mainly found in blood secretion?

A

IgM and IgG

74
Q

If B cells fail to find an antigen, or fails to find the appropriate Th cell when in the secondary lymphoid organ (lymph node) what happens?

A

They leave nodes via the efferent lymphatics and move on to the next node.

75
Q

How many antigen binding receptors on B and T cells, can mammals express/ produce?

A

Up to 10^15

76
Q

Where is all the information needed to make proteins, including antigen receptors located?

A

In the Genome

77
Q

How many genes do mammals use?

A

Fewer than 500

78
Q

What determines the ability of a receptor to bind an antigen?

A

Its shape, ( this determines folding of its peptide chain and amino acid sequences.)

79
Q

What accounts for gene diversity in B cells?

A

Gene recombination
Somatic mutation
Gene conversion

80
Q

How many genes code for the constant region on antigens?

A

1 gene

81
Q

What is one of the most important mechanisms of deleting unwanted genes?

A

Looping out

82
Q

What types of light chain are possible?

A

Gamma and Lambda

83
Q

How many attempts at gene rearrangement do B cells have to code for a functional immunoglobulin? What happens if all attempts fail?

A

4 attempts. Apoptosis occurs if not productive by 4th attempt.

84
Q

How many CDR’s do immunoglobulins have?

A

3 CDRs

85
Q

How are the CDR’s generated?

A

CDR 1 and 2 are generated by somatic mutation.
CDR3 is generated by gene conversion.

86
Q

What is gene conversion?

A

The insertion of pseudogenes into a single variable region to generate sequence diversity.

87
Q

What can happen if the regulation of the adaptive immune response is not working?

A

Autoimmunity
immunodeficiency/ immunosuppression

88
Q

TRUE or FALSE: T and B cells generate self antigen receptors (about 50 %)

A

TRUE
They must be destroyed/ turned off so they dont cause autoimmunity.

89
Q

What is tolerance?

A

The lack of an immune response to a specific antigen.

90
Q

TRUE or FALSE: Immature lymphocytes become tolerant to an antigen only if they first meet in early adulthood.

A

FALSE- Immature lymphocytes become tolerant to an antigen only if they first meet in fetal life.

91
Q

Which cells (T or B cells )are rendered more tolerant more easily ? Which cells remain tolerant longer?

A

T Cells
T cells

92
Q

What accounts for gene diversity in T cells?

A

Gene conversion

93
Q

What are important characteristics of central T cell tolerance?

A
  • Occurring in immature T cells-?
  • No functional T cells with receptors that can bind to self antigens
  • 2/3 of possible gene arrangements will be out of frame ( Cells with Non functional TCRs will undergo apoptosis(Negative selection))
  • Thymic epithelial cells express many proteins from different tissues
  • AIRE= transcription regulator, autoimmune regulated.
  • Positive selection ensures that cells recognize self- MHC molecules survive.
94
Q

What are important characteristics of peripheral T cell tolerance?

A
  • occurring in mature T cells
  • aclonal anergy
95
Q

What organ induces central T cell tolerance by negative selection?

A

Thymus.

96
Q

What causes positive selections with T cell tolerance?

A

T cells that survive because they are un-reactive to auto antigens but still respond to antigenic peptides in association with MHC molecules are allowed to proliferate and become MHC restricted non-self reactive T cells via positive selection.

97
Q

What is clonal anergy?

A

The prolonged suppression of T cell function. T cells require multiple signals in order to respond to an antigen. If the signals are insufficient or inappropriate, T cell responses to an antigen will be suppressed.
Peripheral tolerance through clonal anergy will develop if a TCR is stimulate by antigen in the absence of simultaneous co stimulation through the CD28/ CD80 or CD28/CD86 pathway

98
Q

TRUE or FALSE: A very large dose of antigen will cause a very strong immune response

A

FALSE
Too low or too high of a dose can induce tolerance or immune paralysis (no participation of APC) ( respectively)

99
Q

What are important characteristics of central B cell tolerance?

A
  • VDJ rearrangement, gene conversion, somatic mutation.
  • Immature B cells can recognize self antigens (55%-75%)
  • B cell suppression at early stages in animals development
100
Q

What are important characteristics of peripheral B cell tolerance?

A
  • Absence of costimulation
    repeated exhaustive antigen stimulation = short lived plasma cells, no memory cells = tolerance
  • Oral proteins in high doses induces clonal deletions and anergy
  • Oral proteins in low doses induces development of T reg cells
101
Q

In Central tolerance, immature B cells receiving low doses of antigen …..

A

They will have clonal abortion occur where they will get rid of the antigen without mounting an appropriate immune response since the dose was too low to stimulate the response.

102
Q

In peripheral tolerance, what factors can lead to a mature B cell to clonal exhaustion ( or immune paralysis)?

A

Exhaustive antigen challenge or very high doses of antigen.

103
Q

In peripheral tolerance, what factors can lead to a mature B cell to Functional deletion?

A

Absence of costimulation, excessive suppressor cell activity, excessive T independent antigen.

104
Q

In peripheral tolerance, what factors can lead to a mature B cell to Receptor Blockade?

A

Excessive T independent antigens.

105
Q

What is the main characteristics of the immune response induced by T independent antigens?

A
  • They can only produce one type of antigen (IgM)
  • Main characteristic of T independent antigens - no T helper cells
106
Q

What happens with the presence and absence of antigens?

A

Antigens present - prolonged immune response
Antigens absent- immune response stops

107
Q

Where are Langerhans cells found and what response does it promote?

A

Found in skin, promotes T cell response

108
Q

Where are Follicular dendritic cells found and what response does it promote?

A

Found in lymph nodes, promotes B cell response.

109
Q

What response does dendritic cell 1 ‘s produce? Dendritic cell 2 ‘s produce?

A

Th1 (cellular mediated immune response)
Th2 (antibody mediated immune response)

110
Q

Where are induced iTreg cells found ?

A

In the intestines

111
Q

What are the roles of IL-10 ?

A
  • suppresses macrophages, Th1, Th2, Th17,NK cells, and DC’s. This is all to decrease or stop the immune response.
  • Enhances T reg cells
112
Q

What are the roles of Transforming Growth factor Beta?

A
  • Regulates T cell activation (reducing T cell proliferation and antagonizing IFN-gamma and IL-12),
  • Regulates Macrophages (enhancing integrin expression and phagocytosis, but reduces respiratory burst and cytotoxicity)
  • Regulates B cell function (reduces B cell proliferation, but also promotes IGA production and apoptosis)
  • Other cells
  • M2 Macrophages: induce tolerance, suppress inflammation, inhibit dendritic cell antigen presentation
  • Indolemine 2, 3 Dioxygenase: Tryptophan degradation.
  • Dendritic Cells (DC1, DC2)
  • Natural suppressor cells: suppress B and T cell proliferation, and immunoglobulin production
113
Q

What substances from the CNS interact with the immune system and how?

A
  • Encephalins : Increase Cytotoxic T cells
  • B- endorphin : Increases Cytotoxic T cells and antibody production.
  • a- endorphin: Decrease antibody production
  • Somatostatin: Decrease immune response
  • Somatotrophin: Increase immune response.
114
Q

What is released from the adrenal glands during periods of stress?

A

Steroids, which suppresses the immune system

115
Q

What cytokines are released from the immune system and what is the result of them?

A
  • IL-1, IL-6, TNF-alpha, HMGB-1 ( pro-inflammatory cytokines)
  • Can cause fever, sleep disturbances, appetite.
116
Q

What are characteristics of Type IV hypersensitivity?

A
  • Cellular immune response
  • Delayed hypersensitivity ( it takes 2-3 days to see reaction)
  • Antigen presenting cells
  • T cells
    Ex: Tuberculin: inflammatory response in the skin of an animal infected with tuberculosis following and intradermal injection of tuberculin
117
Q

What are some important things about the Tuberculin test?

A

It is a simple test

  • False positives can occur in animals that have been exposed to Mycobacterium phlei
  • False negatives can occur in animals with advanced Tuberculosis (IgG) or if the animal was tested at an early stage of infection.
  • Cross reactions occur with: Mycobacterium avium, Mycobacterium paratuberculosis (Johne disease), and Nocardia spp
118
Q

What are other skin tests that work the same way as the tuberculin test?

A
  • Johnin - Mycobacterium avium var paratuberculosis
  • Brucella abortus
  • Mallein- Burkholderia mallei
  • Histoplasmin- Histoplasmosis
  • Coccidioidin- Coccidioidomycosis
119
Q

What is allergic contact dermatitis?

A
  • If reactive chemicals are painted onto skin they may bind to skin proteins, and the resulting complexes are processed by langerhans cells in the dermis. These skin cells are now seen as foreign and processed by the langerhans cells
  • High production of IL-12, IL-18, and IL-23 cause overstimulation of cytotoxic T cells (which produces high levels of IFN-gamma)
  • T cells (Cytotoxic) will attack the sensitized epidermal cells and this creates vesicles.
  • Poison Ivy, Chrome/Nickel, Resin/Latex ( examples of allergic contact dermatitis)
120
Q

What is some important information about Allergic contact dermatitis?
List Pathogenesis, clinical signs, distribution, major allergens, diagnosis, pathology, and treatment

A

Pathogenesis: Type IV hypersensitivity
Clinical Signs: Hyperemia, vesiculation, alopecia, erythema.
Distribution: Hairless areas, usually ventral abdomen and feet.
Major allergens: Reactive chemicals/ dyes in contact with skin.
Diagnosis: Delayed response on patch testing
Pathology: Mononuclear cell infiltration, vesiculation
Treatment: Steroids

121
Q

What is some important information about Atopic dermatitis?
List Pathogenesis, clinical signs, distribution, major allergens, diagnosis, pathology, and treatment

A

Pathogenesis: Type I hypersensitivity
Clinical Signs: Hyperemia, uticaria, pruritis
Distribution: Face, nose, eyes, feet, perineum
Major allergens: Foods and pollens, fleas, inhaled allergens.
Diagnosis: Intradermal testing, immediate response.
Pathology: Eosinophilic infiltration, edema
Treatment: Steroids, antihistamines, hyposensitization

122
Q

What is a cell proliferation test?

A

This is a test where you take lymphocytes and expose them to the antigen or mitogen and then place radioactive thymidine into the test tube. Dividing or stimulated cells will take up H3-thymidine. You would then centrifuge the test tube and remove the unbound thymidine.
You must then measure the radioactivity of the remaining cells.

123
Q

What is a test of Cell death?

A

This is a measurement of cell death by detecting the release of Cr-51 by dying cells. This release may be triggered by cytotoxic T cells or NK cells

124
Q

What are the characteristics of Type I hypersensitivity?

A
  • Known as allergies
  • Exaggerated Th2 response
  • Excessive amount of IgE= atopy
  • Affected animals = atopic
  • Genes + environmental factors = allergy
  • Susceptible breeds of dogs
  • Humans-child infections
  • Early contact with allergens less susceptible to allergens.
  • Intestinal microflora
  • Parasite worms.
125
Q

In Type I hypersensitivity when exposed to IgE, what is the reaction caused by FCeRI inn Mast Cells?

A
  • Mast cell degranulation
  • Found in Eosinophil, ADCC, Dendritic cells, and Macrophages
126
Q

In Type I hypersensitivity when exposed to IgE, what is the reaction caused by FCeRII in Mast cells?

A
  • B cell down regulation.
  • Found in Macrophage, phagocytosis, Natural killer cells, dendritic cells, and Eosinophils,
127
Q

In the complement receptor CR2, what is the reaction caused by FCeRII, in B cells, T cells, and Dendritic Cells?

A

B cell stimulation and survival

128
Q

Where can you find mast cells?

A
  • Intestine, skin, airways, and around nerves.
  • They are close to blood vessels
  • Release pro-inflammatory mediators.
129
Q

What substances are released from mast cells of the connective tissue and skin?

A

Histamine and Heparin
Life span > 6 months

130
Q

What substances are released from mast cells of the Intestines and Lungs?

A

Chondroitin sulfate and few histamine
Life span is < 40 days

131
Q

How many IgE receptors are needed to stimulate a mast cell?

A

2

132
Q

How fast does the reaction take place where a mast cell becomes degranulated and causes inflammation?

A

seconds .
Inflammation is the main event in the development of allergic reactions.

133
Q

Besides IgE, what else can cause the stimulation and degradation of mast cells?

A
  • cytokines
  • chemokines
  • chemical agents
  • physical stimuli
  • insect and animal venoms
  • virus
  • DAMPs
  • PAMPS
134
Q

What is released form mast cells during granule exocytosis?

A
  • Histamine
  • Serotonin
  • Tryptase
  • Kallikreins
  • Proteases
  • Proteoglycans
    This occurs over a few seconds
135
Q

What is released form mast cells during Eicosanoid synthesis and secretion?

A
  • Leukotrienes
  • Prostaglandins
  • Platelet Activating Factor
    This occurs over a few minutes
136
Q

What is released form mast cells during Cytokine synthesis and secretion?

A
  • IL-4, IL-5, IL-6, IL-13, TNF- alpha, and MIP-1 alpha
    This occurs over a few hours
137
Q

what Interlukin is very important and a major mediator of type I sensitivity?

A

IL-33

138
Q

What is the clinical signs of mast cell activation and degranulation within the gastrointestinal tract?

A
  • Fluid secretion and peristalsis which will lead to emptying of GI tract ( ie. Vomiting and diarrhea)
139
Q

What is the clinical signs of mast cell activation and degranulation within the respiratory tract?

A
  • Mucus secretion and bronchoconstriction. This can cause difficulty breathing.
140
Q

What is the clinical signs of mast cell activation and degranulation within the blood vessels?

A
  • Increased vascular permeability. This will cause movement of fluids, proteins, and cells out of blood vessels and into inflamed tissue .
141
Q

What receptor will enhance mast cell degranulation?

A

alpha adrenergic receptors (norepi, phenylephrine)
This will also block B adrenergic receptors ( like propranolol)

142
Q

What receptor will inhibit mast cell degranulation?

A

Beta adrenergic receptors ( isoproterenol, epinephrine, salbutamol) EPINEPHRINE IS THE BEST CHOICE
This will also block alpha adrenergic receptors ( norepinephrine, phenylephrine)

143
Q

When giving medications to enhance mast cell degranulation, how long does it take to see an affect?

A

Immediate inflammation occurs in 10-20 minutes.
A late phase reaction occurs after about 6-12 hours

144
Q

What is the affect of Beta adrenergic receptor on mast cells, smooth muscle, and blood vessels?

A

Overall: Alpha blockade
Mast Cell: Suppresses degranulation
Smooth Muscle: Relaxes
Blood Vessels: Dilate

145
Q

What is the affect of alpha adrenergic receptor on mast cells, smooth muscle, and blood vessels?

A

Overall: Beta blockade
Mast Cell: Enhances degranulation
Smooth Muscle: Contracts
Blood Vessels: Constricts

146
Q

What antibody is the one most affected by a incompatible donor in a blood transfusion?

A

IgM

147
Q

What is the reaction to IgM antibodies that occur during an incompatible blood transfusion ?

A
  • Agglutination
  • Opsonization
  • Phagocytosis
  • Hemolysis
148
Q

What can be the main clinical signs in a patient affected with hemolysis from an incompatible transfusion?

A

Anemia
Hemoglobinemia
Hemoglobinuria
Disseminated Blood Coagulation
Complement Activation
Mast cell degranulation

149
Q

What causes hemolysis of RBC in an incompatible transfusion?

A

Antibody and Complement

150
Q

What are the four conditions that must be present in Hemolytic disease of the newborn (HDN) or (Neonatal Isoerythrolysis)?

A
  1. ) Newborn with different blood type than mother.
  2. ) Mother must be sensitized to this red cell antigen
  3. ) Mothers response must be boosted by trans-placental hemorrhage or repeated pregnancies.
  4. ) Newborn animal must ingest colostrum with high Ab against its red cells.
151
Q

What causes Type II hypersensitivity hemolysis from drugs?

A

Drug and antibody and complement system can cause bystander hemolysis.
Drugs attached to red blood cell surface can cause antibody and complement to destroy cell.
Drugs that modify rbc membrane can make it seem foreign and antibodies attach it and destroy via phagocytosis

152
Q

Which infectious diseases cause Type II hypersensitivity reactions that lead to severe anemia?

A

Equine infectious anemia, anaplasmosis, trypanosomiasis, Babesiosis

153
Q

What is Type III hypersensitivity is caused by?

A

Antigen, Antibody, Complement (Immune complex)

154
Q

Where is the immune complex in type III hypersensitivity located?

A

IC is deposited in tissues. Chemotactic peptides are present which attracts more neutrophils

155
Q

What must the animal have in order to produce a high amount of immune complexes to participate in type III hypersensitivity?

A

High amount of antibodies or High amount of Antigen.

156
Q

What are the types of type III hypersensitivity and where are their immune complexes formed?

A

Local type: Immune complexes are formed within the tissue.
Generalized Type: Immune complexes are formed within the blood stream. Complexes are deposited in glomeruli in the kidney. Can cause renal failure.

157
Q

What are some characteristics of Local type III hypersensitivity?

A
  • Injection given SQ
  • high levels of antibodies in blood stream
  • inflammation at injection site
  • Arthus reaction: red edematous swelling, local hemorrhage, thrombosis, and tissue destruction.
  • Reaction normally occurs 6-8 hours after injection. SQ injection.
  • after neutrophils, macrophages populate and then their are high levels of nitric oxide, chemokines, leukotrienes, and cytokines.
    Reversed Arthus reaction can be produced high levels of antigens, and then antibodies are injected SQ and can cause same response.
158
Q

What complement or component is chemotactic for neutrophils?

A

C5a

159
Q

What are examples of local type III hypersensitivity?

A
  • Blue eye ( caused by canine adenovirus type- 1) (will go away after antibody levels decline) (happens as a response after vaccination sometimes)
  • Hypersensitivity pneumonitis ( Saccharopolyspora recctivirgula)
  • Staphylococcal hypersensitivity
160
Q

What are some characteristics of General type III hypersensitivity?

A
  • IV antigen + circulating AB = Immune complex (IC)
  • Located in blood circulation and can be removed by erythrocytes and macrophages.
  • Production of high amounts of IC can be deposited on blood vessels where there is a physiological outflow of fluid: Glomeruli, synovia (joints), and choroid plexus.
161
Q

What prevents the significant accumulation of immune complexes in tissues?

A

Complement components

162
Q

Primates vs. other mammals. What is the binding site for immune complexes related to type III hypersensitivity?

A

In primates: bind to complement receptors on red blood cells.
In other mammals: Immune complexes bind to receptors on platelets.

163
Q

In type III hypersensitivity, if immune complexes bind to vessel walls what will happen?

A

Will be deposited into the arterial intima. Neutrophil accumulation will occur and cause arteritis

164
Q

In type III hypersensitivity, if immune complexes bind to glomeruli what will happen?

A

There will be a proliferative response and it will cause glomerulonephritis

165
Q

In type III hypersensitivity, if immune complexes bind to synovia what will happen?

A

Neutrophil accumulation which will lead to arthritis.

166
Q

What cells can be found in the center of the kidneys?

A

mesangial cells

167
Q

Important Note: Glomerulonephritis

A

Immune complexes contain IgG, IgM, IgA, and C3 and can affect mesangial, sub-endothelial regions, and have dense deposits within glomerular basement. Type III glomerulonephritis do not contain Ig but do contain C3. This will produce inflammation.

168
Q

What doe mesangial and endothelial cell proliferation produce? what effects do these products have?

A

Produce: IL-6, and TGF-B
TGF- B can produce fibrosis on outside of vessel.
Fibrosis will block the normal filtration of blood and urine. So kidney function will become poor/ cause kidney failure.

169
Q

What are some causes of glomerulonephritis?

A
  • equine infectious anemia
  • Infectious canine Hepatitis
  • African swine fever
  • Leishmaniasis
  • Lyme disease
  • Pyometra
  • Chronic pneumonia
  • Bacterial endocarditis
  • Tumors: lymphosarcomas, osteosarcomas, mastocytomas.
170
Q

IgE antibodies are mainly attached to a group of cells. The main one it is attached to is …

A

Mast Cells ( Also basophils)

171
Q

What interlukin is overproduced in Hypersensitivity I?

A

IL-4

172
Q

What does basophils do during the hypersensitivity I reaction?

A

Binds IgE which causes basophil degranulation. This increases vascular permeability.

  • Activation is associated with long term allergic states.
  • Basophils are very important in responding to parasites.
  • Basophils also have role in tick, bacterial, toxic degradation from venoms and will contribute to tumor rejection.
173
Q

What is the roles of eosinophils in type I hypersensitivity?

A

Parasites and pathogens/ PAMPs and DAMPs trigger response.
Eosinophils release:
- Oxidants and enzymes which cause tissue damage and inflammation.
- Lipid Mediators : which cause pain, smooth muscle contraction and mucus production.
- Cationic granule proteins: which causes tissue damage and inflammation
- Cytokines: Which trigger macrophage activation, Dendritic cell activation, neutrophil activation, endothelial cell activation.
- Chemokines: T cell chemotaxis and activation

174
Q

What is the shock organs in the dog? The cat? The Horse? Ruminants? Swine? Chickens? Humans?

A

Dog: Hepatic Veins
Cat: Respiratory tract and intestines
Horse: Respiratory tract and intestines
Ruminants: Respiratory tract
Swine: Respiratory tract and intestines
Chickens: Respiratory tract
Humans: Respiratory tract

175
Q

TRUE OR FALSE: Allergic Anaphylaxis is a mild reaction and only affects local tissues.

A

FALSE: Allergic anaphylaxis is a severe, life threatening systemic hypersensitivity reaction.

176
Q

What is the role of IL-31 in atopic dermatitis?

A

IL-31 makes contact with sensory neurons which cause the itching sensation.

177
Q

How can you diagnose type I hypersensitivity ?

A
  • Intradermal skin testing
  • Passive cutaneous anaphylaxis- you take animals blood, and spin down serum, and then dilute it and inject it SQ into another animal . Next day IV injection of antigen. If you see reaction in subcutaneous location then it is positive for antibodies.
  • Measuring IgE: If level is high, animal is most likely suffering from type I hypersensitivity.
178
Q

What is the treatment of type I hypersensitivity reactions?

A
  • Avoid exposure
  • Corticosteroids
  • Antihistamines
  • B stimulants: epinephrine, isoprenaline, salbutamol
    A antagonists: methoxamine, phenylephrine
    Allergen specific immunotherapy.
179
Q

What will occur if you give animal Allergy specific immunotherapy shots?

A

Class switching. If their is a large amount of IgG in circulation from repeated infection, it will cause competition with IgG / IgE. the allergen will likely have a higher affinity for IgG and thus they will beat out the IgE and the antigens will be targeted for destruction.

180
Q

Canine Atopic dermatitis immunotherapeutic is injectable ( cytopoint). This medication does what?

A

Targets IL-31 and neutralizes it, this will stop itching and inflammation.

181
Q

What is hypersensitivity reaction II?

A

-RBC antigens. Ab + complement= RBC destruction.
Animals may have antibodies to foreign blood group without previous experience.

182
Q

What antibody causes agglutination in blood cell slides?

A

IgM ( 5 molecules) Will be present on RBC membrane

First Year Veterinary School (43 decks)

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