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IMMUNOLOGY > IMMUNO > Flashcards

IMMUNO Flashcards

1
Q

Name the 2 major types of immunity

A

Innate and Adaptive

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2
Q

What are the 2 roles of the immune system?

A
  1. Recognition function

2. Effector function

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3
Q

Describe innate immunity

A

Innate immunity is a “first line of defence”, which is present at birth and responds rapidly, with no specificity and no memory.

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4
Q

Name 3 examples of innate immunity

A
  1. Cells (NK cells, phagocytes, eosinophils)
  2. Barriers (physical / chemical / biological)
  3. Soluble factors (lysozyme, complement, cytokines, acute phase proteins)
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5
Q

List 5 characteristics of the adaptive immune system

A
  1. Highly specific
  2. Has memory
  3. Adpative
  4. Slow to start
  5. Recognition of self from non-self
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6
Q

What are the 2 components of the adaptive immune system?

A
  1. Humoral

2. Cellular

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7
Q

What is the humoral component of the adaptive immune system made up of?

A

Antibodies (immunoglobulins) - specific proteins produced against pathogens, from B lymphocytes

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8
Q

What is the cellular component of the adaptive immune system made up of?

A

B lymphocytes and T lymphocytes

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9
Q

What is an antigen?

A

Any substance that elicits an immune response

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10
Q

What is an epitope?

A

A restricted part of the antigen to which an antibody binds

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11
Q

Give some examples/forms in which antigens present in (x6)

A
  1. Proteins
  2. Carbohydrates
  3. Nucleic Acids
  4. Lipids
  5. Drugs e.g. penicillin
  6. Inorganic molecules (e.g. Nickel)
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12
Q

Name the granulocytes (x3)

A
  • Neutrophils
  • Eosinophils
  • Basophils
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13
Q

How many percent of blood leucocytes does each make up:

  • Neutrophils
  • Eosinophils
  • Basophils
A

neutrophils: 60-70%
eosinophils: 2-5%
basophils:

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14
Q

Size of neutrophils

A

10-20um

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15
Q

Role of neutrophils

A

Phagocytosis and destruction of pathogens

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16
Q

Mode of action of neutrophils

A

Adhere to endothelial cells lining blood vessels and squeeze between them to leave circulation and enter tissues

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17
Q

Mode of action of eosinophils

A

Release of granules upon activation, resulting in the killing of large pathogens that cannot be phagocytosed

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18
Q

What is the function of the mononuclear phagocyte system?

A

Disposal of microbes and dead body cells through phagocytosis

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19
Q

Where in the body is each found?

  • monocytes
  • kupffer cells
  • mesangial cells
  • alveolar macrophages
  • microglial cells
  • sinus macrophages
  • serosal macrophages
A
  • monocytes – blood
  • kupffer cells – liver
  • mesangial cells – kidney
  • alveolar macrophages – lungs
  • microglial cells – brain
  • sinus macrophages – spleen, lymph nodes
  • serosal macrophages – peritoneal cavity
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20
Q

Function of platelets

A

involved in blood clotting and inflammation

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21
Q

function of antigen presenting cells (APC)

A

Present antigen to T cells and produce cytokines

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22
Q

Function of endothelial cells

A

Receptors recognise certain lymphocytes and control lymphocyte traffic and distribution

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23
Q

Name the primary lymphoid organs

A

Bone marrow and Thymus

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24
Q

Name the secondary lymphoid organs (x6)

A
  • Peyer’s patches
  • Lymph nodes
  • Spleen
  • Waldeyer’s Ring
  • Bronchus associated lymphoid tissue
  • Lymphoid nodules
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25
Q

CD marker on Helper T cell surface

A

CD3, CD4

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26
Q

CD marker on Cytotoxic T cell surface

A

CD3, CD8

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27
Q

How many antigenic determinant is each lymphocyte specific for?

A

1

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28
Q

Name the 5 classes of immunoglobulins

A

IgG, IgA, IgM, IgE, IgD

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29
Q

What are the 2 types of light chains?

A

Lambda

Kappa

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30
Q

Which chain determines the class of antibodies?

A

Heavy chain

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31
Q

Which heavy chains of immunoglobulin groups fold into 4 globular domains?

A

IgG, IgA, IgD

VH, CH1, CH2, CH3

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32
Q

Which heavy chains of immunoglobulin groups fold into 5 globular domains?

A

IgM, IgE

VH, CH1, CH2, CH3, CH4

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33
Q

Which is the most abundant Ig in plasma?

A

IgG

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34
Q

Name the subclasses of IgG

A

IgG1
IgG2
IgG3
IgG4

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35
Q

Which class of Ig can pass from mother to child through placenta?

A

IgG

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36
Q

Which class of Ig is the predominant antibody of secondary response?

A

IgG

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37
Q

What does IgG do?

A

IgG is very efficient at triggering complement and phagocytosis via Fc receptors

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38
Q

Name the subclasses of IgA

A

IgA1

IgA2

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39
Q

Name the two forms in which IgA can be present as

A

Monomeric

Dimeric

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40
Q

Describe the composition of serum IgA

A

Monomeric, with 90% IgA1 and 10% IgA2

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41
Q

Describe the composition of secretory IgA

A

Predominantly dimeric, with 40% IgA1 and 60% IgA2

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42
Q

Which is the major antibody in seromucous secretions?

A

IgA

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43
Q

Where can IgA be found?

A

Seromucous secretions e.g. milk, saliva, gut

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44
Q

Which is the class of antibody first encountered by invading bacteria and viruses?

A

IgA

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45
Q

What is the Fc region of antibody?

A

Fragment crystallisation region

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46
Q

What is the Fab region of antibody?

A

Fragment antigen-binding region

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47
Q

Where is IgM present?

A

Only in plasma

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48
Q

Why is IgM only present in plasma?

A

It is too large to enter tissues

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49
Q

Which is the predominant antibody of primary response?

A

IgM

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50
Q

How are the 5 Y shaped units of IgM joined?

A

J chain and disulfide bridges

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51
Q

What does IgE interact with?

A

FceRI - binds Fc region of IgE

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52
Q

Where is FceRI expressed?

A

Mast cells and basophils

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53
Q

What is IgE important for?

A

Protects against parasitic infections

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54
Q

Where is IgD found?

A

On the surface of lymphocytes

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55
Q

What does binding of antibody-coated targets to FcR on immune cells result in? (x5)

A
  1. Phagocytosis
  2. Release of activated oxygen species and enzymes
  3. Release of inflammatory mediators (e.g. histamines)
  4. Enhanced antigen presentation
  5. Clearance of immune complexes
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56
Q

List some functions of the complement system (x6)

A
  1. Triggering and amplification of inflammatory reactions
  2. Attraction of phagocytes by chemotaxis
  3. Clearance of immune complexes
  4. Cellular activation
  5. Direct microbial killing
  6. Important role in the development of antibody responses
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57
Q

3 Pathways in which complement activation can take

A
  1. Classical
  2. Alternative
  3. Lectin
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58
Q

What do the 3 complement activation pathways have in common?

A

They all involve the activation of C3, which is the most abundant and most important of the complement proteins

59
Q

Name the first component of the classical pathway of complement activation

A

C1q

60
Q

Describe the structure of C1q

A

Hexavalent, with a molecular weight of ~460kDa and has a “bunch of tulips”arrangement of 18 polypeptides (3pp/head) –> 6 collagenous base and arm (stalk) regions connected to 6 globular heads

61
Q

Which immunoglobulin(s) can activate complement?

A

IgG and IgM
IgM is the most efficient activator, but only surface bound IgM can activate (unbound IgM in plasma does not activate complement)
IgG1 & IgG3 are strong complement activators; IgG4 does not activate as it is unable to bind the 1st component of the classical pathway

62
Q

Which pathway do immunoglobulins use to activate complement?

A

Classical

only surface bound IgG and IgM

63
Q

List the next steps that occur after binding of immunoglobulins to C1q

A
  • C1r and C1s bind to C1q. They are proteolytic enzymes and cleaves C4 & C2 –> Forms C3 convertase
64
Q

What does C3 convertase do?

A

Breaks down C3 to C3a + C3b

65
Q

What utilizes the alternative pathway to activate complement?

A

Many types of micro-organisms (e.g. bacteria, yeast, trypanosomes)

66
Q

Which of the complement pathways can be used as the first major line of defence against systemic infections?

A

Alternative pathway

67
Q

How is the Lectin pathway activated?

A

Activation by the binding of Mannose-Binding Lectin (MBL) to a micro-organism

68
Q

Describe the Lectin pathway in complement activation

A

Mannose-binding lectin (MBL) binds to pathogen surface, MASP-2 binds and C4 is cleaved

69
Q

What happens after C3b is formed? (x2)

A
  • Opsonisation – Refers to the coating of micro-organisms by antibody or complement components, as phagocytes have receptors for C3b
  • Lysis – Cleaves C5 to C5a + C5b. C5b binds to the surface of micro-organisms, allowing 4 other proteins (C6, C7, C8 & C9) to bind
70
Q

What makes up the MAC complex

A

C5b, C6 to C9

71
Q

What does IgE bind to?

A

Mast cells

72
Q

What is opsonisation?

A

Opsonisation refers to the coating of micro-organisms by antibody or complement compounds, to allow recognisation by phagocytes, which have receptors for C3b

73
Q

What is anaphylaxis?

A

An acute allergic reaction to an antigen to which the body has become hypersensitive

74
Q

Name 2 anaphylatoxins

A

C3a and C5a

75
Q

Mode of action of C3a

A

C3a binds to receptors on mast cells resulting in the release of histamine, causing an increase in vascular permeability, leading to a recruitment of other components of inflammatory response to infection site.

76
Q

Effects of anaphylatoxins

A

Act directly on local blood vessels, increasing blood flow and vascular permeability

77
Q

Mode of action of C5a

A

C5a triggers phagocyte chemotaxis by binding to C5a receptors on phagocytes. (Phagocytes migrate up concentration gradient of C5a to the infection site and become stickier)

78
Q

What are MHC molecules?

A

MHC molecules refer to pathogen-derived peptides delivered to and presented at cell surface by specialised glycoproteins

79
Q

Name the members of MHC Class I family

Name the members of MHC Class II family

A

Class I: HLA-A, HLA-B, HLA-C

Class II: HLA-DP, HLA-DQ, HLA-DR

80
Q

Where are the members of MHC Class I family expressed?

Where are the members of MHC Class II family expressed?

A

Class I: expressed on all nucleated cells, including leucocytes
Class II: expressed only on leucocytes which present antigen to T cells (dendritic cells, macrophages, B cells)

81
Q

What are the antigen receptors on:

  • B cells
  • T cells
A

B cells: surface immunoglobulins

T cells: T cell receptor (TCR)

82
Q

To whom do MHC presents antigenic peptides to?

  • MHC Class I
  • MHC Class II
A
  • MHC Class I - Present peptides to Tc cells

- MHC Class II - Present peptides to Th cells

83
Q

What cell surface proteins do Tc and Th recognise?

A

Tc: CD3 + CD8
Th: CD3 + CD4

84
Q

What gene segments do VH domains contain

A

V (variable)
D (diversity)
J (joining)

85
Q

What gene segments do VL domains contain?

A

V (variable)

J (joining)

86
Q

What gene segments does the constant domain contain?

A

C (constant) genes

87
Q

Actions of the activated Tc cell after binding antigen (x3)

A
  1. Release perforins which form pores in target cell
  2. Release other damaging enzymes
  3. Release cytokines (e.g. TNF; IFN)
88
Q

What does tumour necrosis factor (TNF) do?

A

TNF triggers apoptosis, aided by IFN

89
Q

What distinguishes the 2 classes of T cells

A

The expression of different cell surface proteins.
Tc cells express CD8 –> recognised by MHC Class I proteins
Th cells express CD4 –> recognised by MHC Class II proteins

90
Q

Which is the first antibody class produced?

A

IgM

91
Q

What produces immunoglobulins?

A

B cells

92
Q

What is hypersensitivity?

A

Hypersensitivity refers to an exaggerated inappropriate immune response that sometimes results in inflammatory reactions and tissue damage

93
Q

Which immunoglobulin is Type I hypersensitivity commonly caused by?

A

IgE

IgE binds to FceRI on mast cells in response to innocuous environmental antigens

94
Q

Treatment of mild Type I hypersensitivity (x4)

A
  1. Avoidance
  2. Anti-histamines
  3. Desensitisation
  4. Sodium chromoglycate (stabilises mast cells)
95
Q

What classification of hypersensitivity is reaction to anaesthetics under?

A

Type I hypersensitivity

96
Q

What is Type II Hypersensitivity?

A

Antibody-dependent cytotoxic hypersensitivity

97
Q

What type of hypersensitivity is antibody-dependent cytotoxic hypersensitivity?

A

Type II Hypersensitivity

98
Q

How long does symptoms Type II hypersensitivity take to manifest?

A

12-18h

99
Q

Cause of Type II Hypersensitivity

A

Occurs when IgG/IgM binds to either a self-antigen or a foreign antigen on cells, which leads to phagocytosis, killer cell activity or other cell-mediated lysis

100
Q

Examples of Type II hypersensitivity

A
  1. Blood transfusion of incompatible blood (ABO)

2. Haemolytic disease of new born - result of incompatibility of RhD blood antigens to RhD -ve mother

101
Q

What is Type III Hypersensitivity mediated by?

A

Persistence and deposition of antibody-antigen immune complexes

102
Q

List 4 factors that influence the clearance of immune complexes

A
  1. Dose of antigen
  2. Size of immune complexes
  3. Route of antigen exposure
  4. Binding of antigen directly to tissues
103
Q

What is Type IV hypersensitivity mediated by?

A

T cells and macrophages

104
Q

What is the difference between Type I-III Hypersensitivity VS Type IV hypersensitivity?

A

Type I - III are antibody mediated;

Type IV is mediated by T cells and macrophages

105
Q

What are the 3 types of Type IV Hypersensitivity? How long does each take to develop?

A
  1. Contact (48-72h)
  2. Tuberculin (48-72h)
  3. Granulomatous (21-28days)
106
Q

Which type of hypersensitivity does allergy to dental materials trigger?

A

Type IV Hypersensitivity

107
Q

What are the 2 phases of Type IV Hypersensitivity?

A
  1. Sensitisation (Antigen encountered by dendritic cell in skin - migrates to lymph node and presents antigen to CD4+ T cell)
  2. Elicitation (Antigen subsequently encountered and triggers memory T cells, leading to inflammation)
108
Q

When does autoimmunity occur?

A

Autoimmunity occurs when the self-tolerant mechanisms of the immune system breaks down

109
Q

What happens when autoimmunity occur?

A

Autoreactive antibodies and autoreactive T cells develop. These recognise self antigens i.e. normal components of the body.

110
Q

Name an organ specific autoimmune disease

A

Hashimoto’s thyroiditis

111
Q

Name a non-organ specific autoimmune disease

A

SLE (Systemic lupus erythematosus)

112
Q

Treatment of autoimmune diseases (x4)

A
  • Metabolic control (e.g. anti-thyroid drugs in Graves’ disease)
  • Anti-inflammatory drugs (corticosteroids / non-steroidal anti-inflammatory drugs NSAIDs)
  • Immunosuppressive drugs (e.g. cyclosporine - risk of individual being susceptible to disease as whole immune system cannot be activated)
  • Monoclonal antibodies - to block certain cytokines or their receptors
113
Q

Define immunodeficiency

A

Immunodeficiency refers to the absence or failure of the normal function of the immune system, resulting in increased susceptibility to infection.

114
Q

What can B cell immunodeficiency cause?

A

Recurrent pyogenic infections e.g. pneumonia, sinusitis, otis media

115
Q

Treatment of B cell immunodeficiency

A

Intravenous replacement therapy with immunoglobulin

116
Q

Causes of T cell immunodeficiencies (x4)

A
  • MHC defects
  • CD40 ligand deficiency
  • CD3 mutations
  • Decreased T cell number
117
Q

What can people with T cell immunodeficiency suffer from?

A

High susceptibility to opportunistic infections e.g. candida, Herpes

118
Q

Specific VS non-specific immunodeficiency

A

Specific: Involves abnormalities of B or T cells

Non-specific: Involves abnormalities in complements or phagocytes

119
Q

Primary VS secondary immunodeficiency

A

Primary: Due to intrinsic defects, often genetic or age-related decline
Secondary: Results from extrinsic factors such as drug therapies for cancer/autoimmune diseases; irradiation; organ or bone marrow transplantation; malnutrition; alcoholism

120
Q

What does AIDS and HIV stand for?

A

AIDS: Acquired immunodeficiency syndrome
HIV: Human immunodeficiency virus

121
Q

Name a disease caused by complement deficiency

A

HAE (Hereditary Angioedema)

122
Q

What is hereditary angioedema caused by?

A

Results from a deficiency (absence/dysfunction) in the main inhibitor of the classical pathway, C1 inhibitor

123
Q

What are the long term treatments of hereditary angioedema (HAE)?

A
  1. C1 INH
  2. Danazol
  3. Antifibrinolytic agents
124
Q

What should be done to treat patients suffering from HAE?

A

Administer C1 INH concentrate (oedema should be resolved in 30mins-2h)

125
Q

What should be done to prevent an episode of oedema from a known patient with Hereditary angioedema?

A
  • Danazol for 5 days before and 2 days after procedure (100-600mgs)
  • C1 INH concentrate (500-1500 units) up to 24h beforehand dental procedure
126
Q

Name the phagocytes

A

Neutrophils
Monocytes
Macrophages

127
Q

List 3 genetic defects in phagocytes

A
  1. Chronic granulomatous disease (CGD)
  2. Leucocyte adhesion deficiency
  3. Chediak-Higashi syndrome
128
Q

What happens when autoantigen is localised to a particular organ?

A

Type II hypersensitivity and cell mediated reactions; resulting in damage due to complement activation and phagocyte degranulation

129
Q

What could Type III hypersensitivity cause?

A

Acute tissue damage (in SLE)

130
Q

What type of disorder is Sjogren’s Syndrome?

A

A chronic inflammatory autoimmune disorder

131
Q

What happens in Sjogren’s Syndrome?

A

Lymphocytic infiltrate in salivary and lacrimal glands, resulting in slow destruction and replacement of glandular tissue with fibrotic tissue

132
Q

What does Sjogren’s syndrome cause? (x2)

A
  • Lack of saliva (results in dental caries, oral candida)

- Lack of tear secretion

133
Q

Name an anti-inflammatory drug and its use

A

Corticosteroid / Non-steroidal anti-inflammatory drugs (NSAIDs)
Used in treatment of autoimmune disorder

134
Q

What is the most effective treatment of autoimmune disorders? How do they work?

A

Monoclonal antibodies; they block certain cytokines or their receptors, thus inhibiting immune response and alleviates symptoms

135
Q

What is the disadvantage in using immunosuppressive drugs for treatment of autoimmune disorders?

A

There is a risk of the individual being susceptible to other diseases as the whole immune system is suppressed and cannot be activated

136
Q

How is AIDS/HIV transmitted? (x5)

A
  1. Sexual contact
  2. Sharing of needles - intravenous drug use
  3. Transfer via placenta or milk from mother to child
  4. Blood transfusion
  5. Needlestick injuries
137
Q

What is HIV infection controlled with?

A

Highly active anti-retroviral therapy (HAART), which is a combination of nucleoside analog reverse transcription inhibitors and non-nucleoside RT inhibitor or protease inhibitor

138
Q

Which disease is associated with NADPH oxidase defects? What is this enzyme responsible for?

A

Chronic Granulomatous Disease (CGD); NADPH oxidase is responsible for the generation of superoxide anions (O2-), which normally help phagocytes kill ingested bacteria and fungi.

139
Q

Which disease is associated with a lack of integrin subunit? What results from this?

A

Leukocyte Adhesion Deficiency; Results in repeated pyogenic infections

140
Q

Which disease is associated with a mutation in a gene that regulates lysosome trafficking?

A

Chediak-Higashi syndrome

141
Q

What occurs when antigen is encountered by B/T cells?

A

Clonal selection

142
Q

What provides protection against microorganisms inside cells?

A

T cells (Cytotoxic T cells kill infected cells)

143
Q

Which antibody is present mainly as a surface receptor on B cells?

A

IgD

144
Q

What does HIV bind to?

A

CD4 receptors

IMMUNOLOGY (1 decks)

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