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PVS > Immunology 2 > Flashcards

Immunology 2 Flashcards

1
Q

Define antigen

A

Anything that causes an immune response, usually foreign material but can be our own tissues

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2
Q

Define hapten

A

A small chemical group that lone is non-immunogenic, but when attached to a larger carruer protein can act as an antigenic determinant and elicit antibody or cellular immune responses

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3
Q

Define carrier

A

Foreign proteins to which small non-immunogenic molecules (haptens) can be coupled to stimulate an immune response. Self proteins can serve as carriers

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4
Q

Define adjuvant

A

Any substance which , when mixed with an antigen, enhances the immune response to that antigen (common in vaccines)

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5
Q

What is the importance of antigenic drift and shift?

A

Allows variation and therefore improved immune response evasion. Pathogens exist as multiple strains

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6
Q

Describe antigenic drift

A
  • Point mutations in DNA, lead to coding change in amino acid
  • Subtle variation in protein structure
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7
Q

Outline the effect on immune response to a pathogen that has undergone antigenic drift

A
  • Some antibodies bind to antigens which are unchanged, giving partial protection
  • No antibodies recognise drifted epitope
  • Therefore immune response is partially, but not fully protective
  • Modulation of clinical signs as pathogenic particles are reduced but not cleared
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8
Q

Outline the process of antigenic shift

A
  • Co-infection of 2 viruses which then exchange genetic material
  • Reassortment of segments in genome between different strains of same pathogen
  • Leads to dramatic changes in protein expressed
  • change is radical
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9
Q

What are the consequences for the immune response to a pathogen that has undergone antigenic shift?

A
  • Protein not recognised by antibodies

- Immune response not protective

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10
Q

In what situations is antigenic shift particularly important?

A

Where individuals live in close proximity

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11
Q

What are the consequences of antigenic shift and drift?

A
  • Clinical disease more severe
  • Multiple (consecutive) infections with the same pathogen
  • Mild epidemic due to drift
  • Pandemic due to shift
  • Difficulty regarding vaccination
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12
Q

What are the different types of vaccine that can be used?

A
  • Inactivated pathogen
  • Modified live pathogen
  • Immune stimulating complexes (liposomes)
  • Individual purified recombinant proteins
  • +/- adjuvants
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13
Q

What is the role of Th1 cytokines?

A

Enhance the cell mediated (cytotoxic) response

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14
Q

What is the role of Th2 cytokines?

A

Enhance differentiation of B cells into plasma cells and therefore the antibody (humoral) response

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15
Q

Name the antigen presenting cells

A
  • Dendritic cells
  • Macrophages
  • B-cells
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16
Q

Which APCs are involved in the naive or the primed immune reponse?

A
  • DCs involved in both

- Macrophages and B cells involved in primed only

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17
Q

Which APCs present to naive or memory T cells?

A
  • DCs present to both

- Macrophages and B cells present only to memory T cells

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18
Q

What method of antigen capture is used by which APCs?

A
  • DCs and macrophages use multiple methods

- B cells only by B cell receptor

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19
Q

What is the importance of the location of the lymphocyte regarding immune response development?

A
  • Location and whether naive or primed cell dictates where the immune response develops and its speed
  • Affects vaccines
  • E.g. if vaccine given IM but the pathogen invades at mucosal surface, this is not ideal
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20
Q

Explain why the primed immune response is more efficient than the naive response

A
  • In naive, DCs captre antigen, travel to local lymph node, where will then activate T cells
  • In primed, antigen can be captured, processed and presented locally and efficiently e.g. by MALT
  • Memory cells present in body, more sensitive to restimulation, produce cytokines more quickly = more efficient
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21
Q

What method of antigen capture do B cells use?

A

Binding to sIg and endocytosis (extracellular virus or bacteria)

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22
Q

What method of antigen capture do macrophages use?

A

Phagocytosis (but this is inefficient with soluble antigens. Extracellular)

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23
Q

What method of antigen capture do dendritic cells use?

A

Non-specific macropinocytosis and phagocytosis (efficient with soluble antigens from extracellular fluid)

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24
Q

Give the processing method, MHC restriction, predominant outcome and location of response for a vaccine consisting of an inactivated whole virus, administered IM

A

Processing: Exogenous
MHC: II
Outcome: Antibody response
Location: systemic

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25
Q

Give the processing method, MHC restriction, predominant outcome and location of response for a vaccine consisting of a live whole virus administered IM

A

Processing: endogenous
MHC: I
Outcome: cytotoxic T cell activation
Location: systemic

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26
Q

Give the processing method, MHC restriction, predominant outcome and location of response for a vaccine consisting of a viral vector encoding a single pathogen protein administered IM

A

Processing: endogenous
MHC: I
OUtcome: cytotoxic T cell activation
Location: systemic

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27
Q

Give the processing method, MHC restriction, predominant outcome and location of response for a vaccine consisting of ISCOMS administered IM

A

Processing: endogeous
MHC: I
Outcome: cytotoxic T cell activation
Location: systemic

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28
Q

Give the processing method, MHC restriction, predominant outcome and location of response for a vaccine consisting of recombinant, inert protein administered IM

A

Processing: exogenous
MHC: II
Predominant outcome: antibody
Location: systemic

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29
Q

Give the processing method, MHC restriction, predominant outcome and location of response for a vaccine consisting of live whole virus administered intranasally

A

Processing: endogenous
MHC: I
Outcome: cytotoxic T cell activation
Location: local (mucosal)

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30
Q

Give the processing method, MHC restriction, predominant outcome and location of response for a vaccine consisting of inactivated whole virus administered intranasally

A

Processing: exogenous
MHC: II
Outcome: antibody
Location: local (mucosal)

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31
Q

What are ISCOMS?

A

Immune Stimulating Complexes

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32
Q

Outline the veterinary relevance of antibodies

A
  • Vaccine responses
  • Diagnostics
  • Immune mediated diseases
  • Immunodeficiency
  • Tolerance
  • Protection of neonate via passive immune transfer
  • Therapeutic monoclonal antibodies
  • Monitoring for presence of disease
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33
Q

What immunoglobulins are present on B cells?

A
  • IgM
  • IgD
  • Are attached to the surface
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34
Q

What immunoglobulin is secreted by plasma cells?

A

IgG

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35
Q

What are the 3 signals required for the activation of naive B cells?

A
  • Binding of antigen to surface Ig and internaisation
  • Molecular interaction with Th2 cells
  • Costimulation by cytokines from Th2 cells
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36
Q

What does the presence of IgM indicate regarding the phase of the antibody response?

A

Indicates that the acute phase of antibody response is occuring

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37
Q

What happens to the B cell immunoglobulins once the cell is activated?

A

IgM replaced by IgD

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38
Q

What events occur in B cells following activation?

A
  • Class switching
  • Clonal proliferation
  • Transformation into lymphoblasts then plasma cells
  • Formation of memory cells
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39
Q

What cytokines promote the antibody synthesis by plasma cells?

A

Il-6, Il-11

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40
Q

What region of the receptor is altered in class switching?

A

Only the Fc region, antigen recognition is the same

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41
Q

Where are multiplying plasma cells found?

A

In germinal centres of lymph nodes

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42
Q

Where do the final stages of B cell maturation take place?

A

Ileal Peyer’s patches (ruminant and dog) or the Bursa of Fabricius in birds

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43
Q

Where does antigen presentation take place in the lymph node?

A

In the light zone of the germinal centre

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44
Q

Describe the appearance of plasma cells

A
  • Typical acentric nucleus

- Basophilic

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45
Q

Outline the immunological characteristics of memory B cells

A
  • More rapid Ab synthesis
  • Increased Ag affinity
  • Increased expression of MHC class II and co-stim molecules
  • Interact with armed T cells at lower Ag dose
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46
Q

What determines the class of immunoglobulins?

A

The Fc region’s arrangement of carbohydrate groups

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47
Q

Which immunoglobulins can form multimers? hat is the benefit of multimers?

A
  • IgM and IgE

- Improve binding to antigens and phagocytes

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48
Q

What is the consequence of alterations in the Fab region of immunoglobulins?

A

Alters the binding specificity of the antibody for the antigen

49
Q

What are the functions of the Fc region of immunoglobulins?

A
  • Actively transport Ig to specific locations
  • Bind to complement and promote opsonisation
  • IgG Fc region can bind to PMNLs (neutrophils), macrophages, host tissues facilitating phagocytosis
50
Q

List the functions of antibodies

A
  • Soluble Ab binds pathogen/toxin directly
  • Formation of Ag-Ab complexes
  • Free antibody binds to cell antigens
  • Antibody on surface of B cells binds
51
Q

What is the result of a soluble antibody binding directly to a pathogen/toxin?

A

Pathogen is neutralised and so further infection is blocked

52
Q

What are the results of Ag-Ab complex formation?

A
  • Opsonisation by complement leading to phagocytosis
  • Binding to FcR on phagocytes leading to phagocytosis
  • Persistence may damage organs (thrombus formation)
  • Crosslinking of IgE receptors leading to degranulation of mast cells (more allergic symptoms)
53
Q

What is the result of antibodies binding to antigens on cells?

A

Recognition by specialised lymphocytes leading to cytotoxicity

54
Q

What is the result of an antibody on the surface of B cells binding to antigens?

A

Exogenous antigen presentation to Th2 cells, promotes plasma cell formation

55
Q

What is the chicken equivalent of IgG?

56
Q

Describe the functional relevance of IgG immunoglobulins (where predominates, type of immune response, functions)

A
  • Secondary immune response
  • Dominant in serum
  • Transudates into tissues
  • Fixes complement
  • Binds to FcR
  • Opsonisation
  • Neutralises toxins/pathogens
  • Diagnostic
57
Q

Describe the functional relevance of IgA immunoglobulins (where predominates, type of immune response, functions)

A
  • Mainly mucosal surface, also serum and secretions
  • Prevents conlonisation
  • Can neutralise
  • Weak opsonin
58
Q

Describe the functional relevance of IgM immunoglobulins (where predominates, type of immune response, functions)

A
  • Pirmary immune response
  • Serum dominant
  • Large so can’t transudate easily
  • Fixes complement
  • Effective agglutination
  • Diagnostics
59
Q

Describe the functional relevance of IgE immunoglobulins

where predominates, type of immune response, functions

A
  • Serum and tissues
  • Anti-endoparasitic response
  • Binds via FcR to mast cells and basophils
  • Involved in Type I hypersensitivity
60
Q

Describe the functional relevance of IgD immunoglobulins

A

Rare, expressed only on the surface of naive B cells

61
Q

What is meant by the primary antibody response?

A

The first encounter with the pathogen i.e. B cells are naive

62
Q

What is meant by the secondary antibody response?

A

The encounter of a “known” pathogen i.e. B cells are primed

63
Q

What immunoglobulins predominate in the primary response?

64
Q

What immunoglobulins predominate in the secondary response?

65
Q

What occurs in relation to the memory cells in a secondary response?

A
  • Activation of memory cells

- Differentiate into effector cells

66
Q

Compare the primary and secondary response to a pathogen

A
  • Secondary (aka anamnestic) is quicker, greater magnitude, longer duration
  • IgG in secondary, IgM in primary
  • Primary initiated in local lymph nodes but secondary in local lymphoid tissues
  • In both, memory cells are established
67
Q

What is meant by seroconversion?

A

Change in predominance of immunoglobulin i.e. switch from IgM in primary, to IgG in secondary

68
Q

Describe the immunoglobulin profile on a B cell following class switching

A

Will only express a single type of immunoglobulin on its surface i.e. after will only have IgG, IgA or IgE

69
Q

Describe the immunoglobulin profile of plasma cells

A

Identical to that of the B cell from which it differentiated

70
Q

Which maternal antibodies delivered by the colostrum remain in the gut and which are absorbed?

A

IgA remains in the gut, IgG absorbed

71
Q

What is the function of passive antibody transfer via colostrum?

A

Provides immunological protection against pathogens to which the mother has been exposed for several months

72
Q

What is the function of colostral IgA?

A

Protects the gut epithelium against bacterial invasion until the newborn’s own IgA production starts

73
Q

Name the immunological components of colostrum

A
  • IgG, (major component), IgA, IgM, IgE
  • Cytokines (e.g. bovine IFNy, TNFa, IL-6, IL-6b)
  • Trypsin inhibitors
  • Lymphocytes, majority T cells
74
Q

What is the function of trypsin inhibitors in colostrum?

A

Prevent protein degradation

75
Q

By what mechanisms can IgG be absorbed from the colostrum?

A

Passive transudate or active transport

76
Q

Describe the active method of IgG transport across the gut epithelium

A
  • IgG transport protein, Fc receptor neonatal (FcRn) expressed on gut epithelium
  • 2 molecules of FcRn bin one molecule of IgG
  • Binding is via Fc region of IgG
  • Endocytosis follows to reach local capillaries
77
Q

List the factors influencing the success of passive immunity transfer

A
  • Type of placenta
  • Infection and vaccination history of mother
  • Maternal immune response to vaccines
  • Concentration of Abs in mother’s serum and hence colostrum
  • Colostrum loss pre-parturition
  • Number of young
  • Teat conformation
  • Vigour of offspring
  • Patency of gut epithelium to antibodies
78
Q

Outline how placental type affects Ig transfer

A
  • More invasive placenta has more transfer during gestation
  • e.g. lots of transfer in primates, minimal transfer across endotheliochorial of dog and cat, but no trasnfer in epitheliochorial (horse) and syndesmochorial ruminant)
79
Q

How can Ig transfer into the neonate be tested?

A
  • Turbidity test using precipitation of Igs
  • Single radial immunodiffusion
  • Latex agglutination
  • Brix refractometer with milk or serum in cows, colostrometer in cows
80
Q

Briefly describe the turbidity test for assessing Ig transfer

A
  • Chemical and serum, quantify with spectrophotometer and standard curve
  • Zinc sulphate, glutaraldehyde, sodium sulphite can be used
81
Q

Briefly describe single radial immunodiffusion for assessing Ig transfer

A
  • More accurate and specific
  • Agar gel, antisreum to IgG and serum
  • Result within 18-24 hours
82
Q

Briefly describe latex agglutination for assessing Ig transfer

A
  • reliable and rapid
  • Latex particles coated with anti-IgG and serum
  • Leads to agglutination
  • Takes ~10 mins
83
Q

How much and in what time frame should calves receive colostrum?

A
  • First feed of 3 litres/10% body weight within 2 hours

- Then similar size feed within 12 hours of birth

84
Q

What is the function of neutrophils in the innate immune response?

A
  • Phagocytosis
  • Release of granules that aid cell destruction
  • Amplification of immune response by release of cytokines leading to chemotaxis
85
Q

What is the function of eosinophils in the innate immune response?

A
  • Release granules (e.g. major basic proteins, enzymes) that that destroy cells
  • Release cytokines to amplify response
  • Mainly for allergens and parasites
86
Q

What is the function of lymphocytes in the innate immune response?

A
  • Only natural killer cells involved in innate immune response
  • Target and lyse cells presenting non-self antigen
87
Q

What is the function of monocytes in the innate immune response?

A

Phagocytic with some antigen presentation

88
Q

What are the main PAMPs of Gram -ve bacteria?

A
  • Mainly LPS
  • Also flagella and peptidoglycan
  • DNA CpG motives (unmethylated)
89
Q

What are the main PAMPs of Gram +ve bacteria?

A
  • Mainly peptidoglycan
  • Lipoteichoic acid, flagella
  • DNA CpG motives (unmethylated in bacteria)
90
Q

What is the role of TNFalpha in inflammation?

A
  • Mainly produced by macrophages
  • Regulation of immune cells
  • Endogenous pyrogen, induces apoptotic cell death
  • Activates vascular endothelium
  • Increases IgG, complement and fluid drainage to lymph
  • activates NNfkappab MAPK pathways
91
Q

Outline the origin and role of IL-6 in inflammation

A
  • Secreted by T cells, macrophages and neutrophils
  • Pro-inflammatory cytokine, anti-inflammatory monokine
  • Lymphocyte activation
  • Antibody production
92
Q

Outline the origin and role of IL-1beta in inflammation

A
  • Neutrophils
  • Activates vascular endothelium
  • Local tissue destruction
  • Stimulates IL-6 production
  • Result of above is increased access for effector cells
93
Q

Outline the origin and role of IL-8 in inflammation

A
  • Released by neutrophils

- Attracts neutrophils, basophils and T cells to site of infection

94
Q

Outline the origin and role of IFNy in inflammation

A
  • Produced by T cells, NTKs
  • Most immune cells have appropriate receptors
  • Upregulates MHCI expression on cells
  • Activates class switching to IgE
  • Activation of macrophages
  • Pro-inflammatory
95
Q

What is required in order for infection by pathogens to occur?

A
  • Entry into host
  • Invasion and colonisation of tissues/cells
  • Evasion of host immunity
96
Q

What are the consequences of infection by pathogens?

A
  • Tissue injury, functional impairment
  • Disease caused by host cell destruction/toxin production
  • Host response to pathogen causing tissue damage and disease
97
Q

Name the innate immune receptors

A
  • Toll-like receptors
  • N-formyl-methionyl receptor
  • Mannose receptor
  • Scavenger receptor
98
Q

What is recognised by toll-like receptors?

A
  • Microbial PAMP

- Ligands

99
Q

What is recognised by N-formyl-methionyl receptors?

A

Microbial chemotactic peptides

100
Q

What is recognised by Mannose receptors?

A

Microbial carbohydrates

101
Q

What is recognised by Scavenger receptors

A

Microbial diacylglycerides

102
Q

Which cytokines inhibit the microbicidal function of macrophages?

A

IL-10, IL-4, IL-5

103
Q

Outline the immune responses to extracellular bacteria

A
  • IgA at epithelial surface blocks attachment
  • Complement activation
  • Adaptive humoral neutralising antibody response
  • Th1 response
  • Stimulation of B cells and antibody by LPS and polysaccharide (T-independent)
104
Q

Outline immune responses to intracellular bacteria

A
  • Innate: macrophages and NK cells

- Adaptive: Th1 and CTLs, delayed hypersensitivity reaction and granuloma formation

105
Q

What cytokines mediate the interactions between phagocytes/NK cells and intracellular bacteria?

A

IL-12, IFNy

106
Q

How may extracellular bacteria evade the immune response?

A
  • Inhibition of complement (sialic acid rich sAgs inhibit alternative pathway)
  • Resistance to phagocytosis (polysaccharide rich capsules)
  • Antigenic variation in surface antigens (e.g. Haemophilus spp LPS variants)
107
Q

How may intracellular bacteria evade the immune response?

A
  • Inhibition of phago-lysosome fusion

- Escape to cytosol (e.g. Listeria spp)

108
Q

Outline the innate immune response to viruses

A
  • Infected tissue production of type I IFNs (TLR recognition of viral DNA and RNA)
  • NK cells active where virus inhibition of MHC class I CTL response or where CTLs not induced
  • Apoptosis,, mediated by host PKR kinase
  • Complement, removal of lipid envelope
  • I.e. is mediated by type I IFNs and NK cells
109
Q

Outline the adaptive immune response to viruses

A
  • Neutralising antibody, prevents virus entry (e.g. IgA) and removes free virus
  • CTLs, MHC-1
  • Antibody and complement mediated opsonisation for phagocyte clearance
  • I.e. mediated by antibodies and CTLs
110
Q

Outline the CTL activity in response to viral infection

A
  • When CTL recognises infected nucleated cell, molecules are released that allow CL to bind with infected cell
  • Perforins punch hole in cell and allow granzymes into cytoplasm = apoptosis
  • Fast Fas-mediated target cell apoptosis
111
Q

Outline immune evasion by viruses

A
  • Inhibition of antigen presentation
  • Antigenic variation e.g. flu virus haemaglutinin
  • Inhibition of interferons
  • Latency or provirus (proviruses integrate DNA into host cell)
112
Q

In what ways may viruses inhibit antigen presentation?

A
  • Inhibition of MHC-I synthesis
  • Decoy MHC molecule production
  • Inhibition of proteosomal activity (Herpesvirus)
113
Q

Outline innate immune response to endoparasites

A
  • Phagocytosis of protozoa

- But helminths generally resistant to phagocytes and complement due to thick tegument

114
Q

Outline adaptive immune response to protozoa

A
  • CTL killing of infected cells
  • Neutralising antibody
  • For those in macrophages (e.g. Leishmania), Th1 CMI and macrophage activation (IFNy)
115
Q

Outline adaptive immune response to helminths

A
  • Th2 mediated immunity (IgE, mast cells, eosinophils)
  • Can also involve Th1
  • Production of neutralising IgG antibodies
116
Q

In what way may increased production aid removal of helminth infection?

A

Helminth less able to penetrate epithelium, increased chance of destruction by eosinophils

117
Q

Outline immune evasionsmethods used by protozoa

A
  • Antigenic variation (different life cycle stages)

- Stimulation of Tregs (immunosuppression)

118
Q

Outline immune evasion methods used by helminths

A
  • Large size, different life cycle stages, thick cuticle
  • Resident in gut or lung
  • Immunosuppressive factors

PVS (23 decks)

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