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Phase 2a NEW > Immunology > Flashcards

Immunology Flashcards

1
Q

Innate immunity

A

Instinctive
Non-specific response
Not dependent on lymphycoytes
Present from birth

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2
Q

Adaptive immunity

A

Specific
Acquired/learned
Memory
Requires lymphocytes and ab

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3
Q

Blood sample consists of

A

Centrifuge forms 2 layers:
Upper - plasma, straw-coloured
Middle - Leukocytes, White fluffy

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4
Q

Leukocytes

A

Lymphocytes
Phagocytes
Auxillary cells

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5
Q

Origin of leukocyte cells

A

Multipotent hematopoietic stem cell (haemocytoblast)

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6
Q

Leukocyte cell differentiation goes through

A

Bone marrow to thymus to blood

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7
Q

Cells of immune system

A 
Polymorphonuclear leukocytes (Neutrophil (neutral stain-liking), eosinophil (acidic-stain liking), basophil (basic-stain liking))
Mononuclear leukocytes (Monocyte (kidney shaped nuclei), T-cells, B-cells)
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8
Q

When monocytes matures through tissues into blood it becomes

A

Macrophage

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9
Q

T cell types

A

T-regs
T-helper
Cytotoxic
Th17

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10
Q

B-cells become activated into

A

Plasma cells

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11
Q

Other leukocytes

A 
Mast cells
Natural killer cells |(specialised T cells)
Dendritic cell
Kupffer cell - liver
Langerhans - skin
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12
Q

Soluble factors

A

Complement
Antibodies
Cytokines and chemokines

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13
Q

Complement

A

Group of 20 serum proteins secreted by liver that need to be activated to be functional
Modes of action - Direct lysis, attract leukocytes to site

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14
Q

Antibodies

A

Immunuglobulins

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15
Q

IgG

A

Y-shaped
Constant and variable regions
Most predominant Ig in human serum - 70-75%

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16
Q

IgM

A

Pentamer-shaped
10% of Ig in serum
Mainly found in blood, too big to cross endothelium
Mainly primary response

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17
Q

IgA

A

15% of Ig in serum
Monomer
Mucous secretions such as saliva
Secretory component sticks them together

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18
Q

IgE

A

0.05% of Ig in serum
Basophils and mast cells
Allergic reactions

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19
Q

Cytokines

A

[roteins secreted by immune and non-immune cells
Interferon - viral infections (alpha, beta and gamma)
alpha and beta - virus infected cells
gamma - activated th1 cells
Interleukins - IL1 (Pro-inflam), IL10 (Anti-inflam)
Colony stimulating factors - stimulate bone marrow to produce leukocyte precursors
TNF alpha and beta - Mediate inflam and cytotoxic reactions

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20
Q

Chemokines

A 
Chemotactic cytokines
Tell leukocytes where to go in body
Group of 40 proteins 
CXCL - Attract neutrophils
CCL - Attract monocytes, lymphocytes, eosniphils, basophils
CX3CL - attract T and NK cells
XCL - attract T cells
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21
Q

Innate immunity

A 
1st line of defence
non-specific
barrier to antigen
instinctive
present from birth
slow response
no memory
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22
Q

adaptive immunity

A

specific to antigen
learnt behaviour
memory to specific antigen
quicker response

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23
Q

Innate immunity cells

A

Neutrophils and macrophages

complement

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24
Q

Innate immunity physical barriers

A

skin
bronchi - mucus, cilia
gut - acid

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25
Q

Inflammatory response

A

breach of barrier (tissue damage or infection during trauma)
Response - coagulation (stop bleeding), acute inflam (leukocyte recruitment), kill pathogens, neutralise toxins, limit pathogen spread, clear pathogens/dead cells, proliferation of cells to repair damage, remove blood clot (remodel extracellular matrix, re-establish normal structure and function of tissue

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26
Q

Inflamamtion

A

Series of reactions that brings cells and molecules of the immune sytem to sites of infection or damage
Hallmarks - Increased blood supply, increased vascular permeability, increased leukocyte extravasation

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27
Q

Acute inflammation

A

complete elimination of a pathogen followed by resolution of damage, diappearance of leukocytes and full regen of tissue

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28
Q

Chronic inflam

A

persistent, un-resolved inflam

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29
Q

Sensing microbes

A

In blood - monocytes, neutrophils
In tissues - Macrophages, dendritic cells
PRR - Pattern recognition receptors (on cells)
PAMP - Pathogen-assocated molecular patterns (on microbe)
PRR bind to PAMP
TLR - Toll-like receptors
Lectin receptors
Scavenger receptor

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30
Q

Complement activation pathways

A

Classical - Ab bound to microbe
Alternative - C binds to microbe
Lectin - activated by mannose-binding lectin bound to microbe

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31
Q

Complement functions

A

Lysis of bacteria directly by MAC
Bond to bacterial membrane and coat it (opsonization)
Chemotaxis

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32
Q

Phagocytosis leukocytes

A

Macrophages, neutrophils, dendritic cells

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33
Q

Mechanisms of microbial killing

A

Oxygen-dependent - ROI (Reactive oxygen intermediates) - superoxides converted to hydrogen peroxide then OH free radical which kills bacterial DNA
Nitrix oxide - vasodilation (viagra) increase extravasation but also anti-microbial.
Oxygen independent - Lysozymes, proteins (defensins insert temslves into membranes), TNF.

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34
Q

Adaptive immunity

A

Antigen specificity and diversity
Immunological memory
Specific non-self recognition

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35
Q

Adaptive immunity

A

Cell mediated T cells - intracelular microbes

Humoral B cells (Ab) - extracellular microbes

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36
Q

Adaptive immunity

A

Thymus - primary lymphid tissue (T cells)
Bone marrow - primary lymphoid tissue (B cells and APCs)
Spleen, lymph nodes, MALT - Secondary lymphoid tissue

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37
Q

Cell-mediated immunity

A

Interlay between APCs and T cells
Requires cell-to-cell contact
Also requires MHC (Major histocompatibility complex) and Instrinsic/extrinsic antigens
Recognise self or non self

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38
Q

T lymphocytes

A

Only respond to presented antigens
T cells that recognise self-antigens are killed in the foetal thymus (T cell selection)
TCR (T cell receptor) recognises foreign antigens in association with MHC

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39
Q

MHC

A

Display peptides from self or non-self proteins

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40
Q

MHC

A

Coded for by HLA genes (Human leukocyte antigen)

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41
Q

MHC 1 and 2

A

MHC 1 - Glycoproteins on all nucleated cells, Displays intrinsic antigens, CD8 Tc cells
MHC 2 - Glycoproteins only on APCs, Displays extrinsic antigens, CD4 Th cells
MHC 3 - Code for secreted proteins (complement)

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42
Q

Link between innate and adaptive immunity

A

MHC

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43
Q

T cell activation

A

T cell then: divides (clonal expansion), differentiates (matured/active), effector functions, memory cells
Can become CD4 (Th) or CD8 (Tc)

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44
Q

Tc activation

A

CD8 + MHC1 = Tc

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45
Q

Th1 activation

A

CD4 + MHC2 = Th1

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46
Q

Humoral adaptive immunity B cell activation

A

B cells express membrane-bound Ig (monomeric - IgM or IgD)

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47
Q

B cells that recognise self are killed in

A

Bone marrow

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48
Q

B cells present Ag to T cells via MHC

A

MHC 2

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49
Q

B cell division is known as

A

Clonal expansion

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50
Q

B cell differentiates into

A 
Plasma cells (AFC - Antibody forming cell)
Memory B cells (Bm)
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51
Q

Lymphoid tissue of the body

A

Neck
Armpit
Groin

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52
Q

Antibody functions

A

Neutralise toxin by binding to it
Increase opsonisation - phagocytosis
Activate complement

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53
Q

Vaccination

A

Tetanus vaccination (tetnaus toxoid from clostridium tatni causes muscle spasms/contractions)

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54
Q

Handling of pathogens

A

Bacteria and fungi - phagocytosis and killing

Viruses - Cellular shutdown, self-sacrifice, cellular resistance

55
Q

Infection is associated with

A

Damage and injury

56
Q

Patterns

A 
Limited characteristics
Gram positive and negative
dsRNA (double stranded)
CpG motifs (DNA nucleotides)
57
Q

Most important PRR

A

Toll-like receptors

58
Q

PRR family

A

Secreted and circulating PRRs

Cell-assocated PRRs

59
Q

Secreted and circulating PRRs

A

Antimicrobial peptides secreted in lining fluids from epithelia and phagocytes (such as defensins and cathelicidins)
Lectins and collectins - carbohydrate-containing proteins that bind carbs or lipids in microbe walls, activate complement and improve phagocytosis
Mannose-binding lectin (deficiency syndromes
Pentraxins - proteins like CRP

60
Q

Cell-associated PRRs

A

Receptors present on cell membrane

61
Q

TLR 3, 7 and 9 respond to

A

Viral infections

62
Q

TLR 4

A

Overactivation can lead to a dangerously high septic response

63
Q

Membrane bound PRRs

A

Mannose receptor on macrophages (fungi)

64
Q

Not all pathogens are extracellular

A

Viruses multiply in cytoplasm of cells

65
Q

Nod-like receptors (NLR)

A

NOD2 - widespread expression, recognises MDP (a breakdown product of peptidoglycan), activates inflammatory signalling pathways. Non-functioning mutation is Crohns disease

66
Q

RLRs

A

Cytoplasmic based receptor for viruses

Rig1

67
Q

Pattern recognition

A

Recognition of microbes and viruses depends on seeing ancient features of them

68
Q

Homeostasis

A

Blood neutrophl members may be dependentupon TLR4 singalling, inpedendent of LPS in homeostasis
Induction of endotoxin tolerance in newborn gyt
maturation of normal immune system
maintaining a balance with commensal organisms

69
Q

Damage recognition

A

TLRs recognise range of endogenous damage molecules

TLR signalling by cellular damage prodcts activates immunity and initate antimocribal signallinh and reapir mechanisms

70
Q

Damage molecules

A

Extracellular molecules - Fibrinogen

Intracellular molecules - Heat shock proteins

71
Q

PRRs in adaptive immunity

A

Activation of TLRs and other PRRs drives cytokine production by APCs that increase likelihood of successful T cell activation
TLR4 agonists used as vaccine adjuvants

72
Q

PRRs and disease

A

recognition of host molecules in autoimmune disease

73
Q

Translation to therapy

A

Enhance TLR signaling - improve immunity with adjuvants

Inhibit TLR signaling - sepsis syndromes, inflammation, arthritis

74
Q

2 greatest public health interventions globally

A

Vaccines

Clean water

75
Q

Poliomyelitis

A

Flu-like symptoms

76
Q

HIV-1 treatment

A

Antiretrovirals (AZT)

77
Q

Ebola

A

Highly contagious
New strains emerge at any time
High death rates
Vaccine under approval after phase 3 trial

78
Q

Smallpox

A

Variolation - scratches on the arm inoculated with pus from a pustule

79
Q

Passive immunisation

A

Transfer of preformed antibodies
Natural - maternal ab across placenta to developing foetus/breast milk. Provides protection against Diptheria, tetanus, rubella, mumps, poliovirus
Artifical - Pooled normal human IgG or immunoserum against pathogens/toxins
Usually during acute danger or infection that could cause serious complications

80
Q

Passive immunisation disadvantage

A

Does not provide immunological memory so no long term protection
Possible allergic reactions to antisera (immunoserum)

81
Q

Uses of passive immunisation

A

Anti-toxins
Prophylaxis
Anti-venins

82
Q

Active immunisation

A

Manipulating immune system to generate peristent proteticve response against pathogens by safely mimicking natural infection

83
Q

Active immunisation

A

Engage innate immune system
Elicit dnger signals and activat immune system, triggers such as PAMPs, TLRs
Activate specialist APC - e.g. Langerhans cells
Engage adaptive immune system - Generate memory B and T cells, activate T cell help

84
Q

Influenza

A

Rapid onset

85
Q

Annual escape variants

A

Require generation of new vaccines

86
Q

Polio

A

Slow onset (3 days)

87
Q

Choices of antigens for vaccine designs

A 
Whole organism - live attenuated pathogen (BCG - for TB vaccines), killed/inactivated pathogen
Subunit - toxoids (toxins)
Peptides
DNA vaccines
Engineered virus
88
Q

Pros and cons for each choice of antigen

A

Transport
Storage
Stability
Cost

89
Q

Whole organism antigen pros and cons

A

Ad - Full natural immune response and memory

Disad - Not advised for immunocompromised patients, ocassionally attenuated organism can revert to viral form also

90
Q

Whole inactivated pathogen pros and cons

A

Ad - No risk of infection, storage is less critical

Disad - Weak immune response and so requires repeated booster vaccinations

91
Q

Subunit vaccines pros and cons

A

Ad - No risk of infection, easy storage

Disad - Weak immune response, repeated boosters required

92
Q

Toxoid

A

Heat treated or chemically modified to eliminate toxicity

93
Q

Capsular polysaccharides

A

Interfere with phagocytes by blocking opsonisation

94
Q

Subunit vaccines

A

Purified proteins - HepB surface antigen (HBsAg)

Recombinant proteins

95
Q

Synthetic peptides as vaccines

A

Peptides can be stimulatory or suppressive

96
Q

DNA vaccines

A

Express genes from pathogens in host cells to generate immune response similar to natural infection
The expression vector is transfected into muscle cells leading to T and B cells memory responses

97
Q

Recombinant vector vaccines

A

Initiate effects of transient infections with pathogen but using a non-pathogenic organism

98
Q

Ebola vaccine

A

Vesicular stomatitis virus relative of rabies virus

99
Q

Adjuvants

A

Substance added to vaccine to stimulate immune system
TLR agonists
Aluminum salts - form precipitates and potentiate opsonised phagocytosis

100
Q

Ideal vaccine should

A

Be safe
Induce suitable immune response
Generrate B and T cell memory
Easy to store and transport

101
Q

Virulence

A

Ability to cause disease once established

102
Q

Invasiveness

A

Capacity to penetrate mucosal surfaces to reach normally sterile sites

103
Q

Virulence factors

A

Microbial factors that cause disease

104
Q

Pathogenicity

A 
Adherence
Evade host defence 
Translocation and invasion 
Evade opsonisation and phagocytosis 
Microbial and host derived factors, can lead to tissue damage
105
Q

Host-pathogen interactions

A

Commensals

Resident flora - overgrowth/translocation can cause disease

106
Q

Opportunistic infections only arise if

A

Immune status becomes altered

107
Q

Microbiome

A

Genome of all microbes (mostly in gut)

108
Q

IBD (Inflammatory bowel disease)

A

Causes decreased gut bacterial diversity
Increased numbers of proteobacteria, decreased numbers of firmicutes and bacteroidetes
Faecal transplantation

109
Q

Ebola main symptom

A

haemorrhagic fevers

110
Q

Viral infections

A

Rapid cell entry

Free virus in blood stream easily neutralised

111
Q

Viral infections - blocks

A

IgA - blocks binding
IgM - agglutinates
Complement - opsonisation and lysis
GAM ab - blocks virus host cell fusion

112
Q

Viral infections - Cell mediated response

A

Interferon - antiviral action
Cytotoxic T lymphocytes - kill infected cells
Natural killer cells and macrophages - further killing

113
Q

Viral infections - body cells affected due to virus

A

Influenza virus to resp epithelium
Varicella zoster virus to skin cells
Yellow fever virus to liver cells

114
Q

Viral evasion

A

Influenza changes coat antigen
HIV and rhinovirus show antigenic variation
Mumps, measles and EBC cause immune suppression

115
Q

Influenza changes in coat antigens reults in

A

Antigenic drift

Antigenic shift

116
Q

Influenza

A 
Spherical particles surrounded by lipid bilayer acquired from infected host cell 
Glycoprotein projections
Haemagglutinin facilitates attachment 
Neuraminidase facilitates viral budding
3 Types - A,B,C
117
Q

HIV - Viral evasion

A

Viral infection of lymphocyte

118
Q

EBV - Viral evasion

A

Cytokine imbalance

119
Q

Adenovirus - Viral evasion

A

Synthesises proteins which bind to MHC

120
Q

Pus

A

Dead white blood cells and bacteria

121
Q

Bacterial infection

A

Enter host via resp, GI, GU tracts and skin breaks

122
Q

Low virulence

A

Phagocytes

123
Q

High virulence

A

Immune response stimulated

124
Q

Extracellular bacteria

A

Antibody response

125
Q

Intracellular bacteria

A

Cellular response

126
Q

Some bacteria produce bacteriocins (peptides) to

A

Kill other bacteria

127
Q

Adhesins

A

Secreted by bacteria to help them bind to mucosal surfaces

128
Q

Biofilms

A

Bacteria can stick together on a surface by secreting an extracellular substance consisting of protein, polysaccharides, and DNA
Helps protect against antimicrobials

129
Q

In TB there is prolonged DTH

A

Continuous macrophage activation forms a granuloma, macrophages adhere together, lytic enzyme release, tissue damage

130
Q

PRR and PAMPs

A

PRR recognise PAMPs but also damage-associated molecular patterns from host cells

131
Q

Bacterial evasion

A

Neisseria - secrete protease lyses IgA
N. Gonorrhoea - Pilli, antigenic variation
Strep pyogenes - M protein inhibits phagocytosis
Mycobacterium - Escape from the phagolysosome

132
Q

Protozoan infection

A

Blood stage - humoral immunity

Tissue stage - cell-mediated immunity

133
Q

Worm infection

A

Helminths
The immune response is not sufficient enough to kill these worms
Interleukin 5 is main mechanism

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