Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Principles > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the immune system?

A

A network of specialised cells, tissues and soluble factors that co-operate to kill and eliminate disease causing pathogens and cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 4 key features of the immune system?

A

1) Specifically identify and respond to ‘non-self’ or ‘abnormal self’
2) Modify response to eliminate different pathogens effectively
3) Promote active tissue repair and healing
4) Immunological memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can happen with an immune over reaction?

A

Allergy or auto immune disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can happen with an immune under reaction?

A

Cancer and infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a constituative barrier and what are the 3 main ones found in the body?

A

A protective barrier formed by the body.

1) Skin
2) Mucus
3) Commensal bacterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the adaptations of the skin to protect the body from infection?

A

1) Physical barrier - tightly packed, highly keratinised, multi layered cells that constantly undergo renewal and replacement
2) Low pH (5.5) and low oxygen tension (bacteria prefer a neutral/basic pH and aerobic conditions
3) Sebaceous glands which secrete hydrophobic oils, lysozyme, ammonia and antimicrobial peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the adaptations of mucus to protect the body from infection?

A

1) Mucus membranes line all body cavities that come int contact with the environment and they can trap invading pathogens
2) Secretory IgA prevents bacteria and virus form attaching and penetrating epithilial cells
3) Contains enzymes (lysozymes, defensins and antimicrobial peptides) which kill invading pathogens
4) Cillia directly trap pathogens and contribute to the removal of mucus assisted by sneezing etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does lactoferrin (found in mucus) do?

A

Starve invading bacteria of iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the adaptations of commensal bacteria to prevent the body from infection?

A

1) Symbiotic relationship with host and reduce pH in colon
2) Produce bactericidins which influence other bacteria
3) compete with pathogens for nutrients
4) Synthesis vitamins (vitamin K and B12)
5) Produce antimicrobial short chain fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

eradication of commensal bacteria with broad spectrum antibiotics can result in opportunistic infections. T or F?

A

True

Candidiasis is common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a primary lymphiod tissue and where are they found

A

Site of leukocyte development

Thymus gland and bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a secondary lympoid tissue and where are they found?

A

SIte where T and B cells are activated by antigens

Lymph nodes, spleen, adenoid (glands in roof of mouth), tonsils, peyer’s patch on small and large intestine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the causes of lymphoedema and why does this increase infection risk?

A

Genetics, cancer treatment (removal of nodes), paracites

Pathogens are trapped in poorly draining lymph which does not pass through lymph nodes to generate an immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 3 types of infection?

A

1) Acute/Limited = rapidly cleared by the immune system giving lasting immunological memory
2) Latent = controlled by the immune system but periodic episodes of pathogen reactivation and replication
3) Chronic = immune response fails (immunodefficiency) giving ongoing pathogen replication.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is direct and indirect communication in the immune system?

A 
Direct = receptor:ligand interactions
Indirect = production and secretion of cytokines by injured or activated immune cells (autocrine, paracrine and endocrine signaling)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is C reactive protein CRP?

A

Major acute phase protein in humans used as a key diagnostic marker in blood test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is CRP produced and how long does it circulate for?

A

Rapid production in the liver

Short half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the functions of CRP?

A

Activate the compliment system
Enhance phagocytosis by opsinisation
*Diagnosis- different serum levels are associated with different levels of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What characterises the innate immune response?

A

Generic and rapid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does the innate immune system recognise a pathogen?

A

Pathogens express PAMPs (pathogen associated molecular patterns)
Innate immune cells express receptors for PAMPs. These are pattern recognition receptors PPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where are PRRs foundas part of innate immune cells?

A

In the cytoplasm and on the cell surface for detection of intra and extracellular pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What type of leukocyte are macrophages?

A

Phagocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What type of leukocyte are natural killer cells?

A

Lymphocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What type of leukocyte are Neutrophils?

A

Phagocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where to macrophages reside?

A

Epithilial tissue eg skin, lungs and intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 5 functions of macrophages?

A

1) Ingest and kill extracellular pathogens by phaocytosis
2) Clear debris from dead and dying tissue- apoptosis
3) Regulate inflammatory response by secreting pro/anti inflammatory cytokines
4) Promote tissue repair and wound healing
5) Antigen presenting cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which pro inflammatory mediators are commonly produced by macrophages?

A

IFN gamma and LPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which bacteria can evade phagosomal killing by macrophages?

A

Salmonella, mycobacterium, Staph aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Some bacteria can evade phagosomal killing by macrophages. How can macrophages kill these bacteria?

A

NK cells secrete pro inflammatory cytokines eg IFN gamma which ACTIVATES macrophages so the produce ROS/RNS and can present antigens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How can macrophages clear dead and dying cells by apoptosis?

A

They have receptors that identify apoptotic cells and when the receptor binds the macrophage is activated => phagocytosis and digestion.
Anti-inflammatory cytokines are released to prevent inflammation as no pathogen is present. This promotes healing and repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What cells do NK cells kill?

A

Infected cells and abnormal cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Do NK cells express PRR on their surface?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do NK cells identify self from non self?

A 
Healthy cells express MHC class 1 proteins containing a self peptide. This binds to an inhibatory protein on NK cells and is identified as self.
Infected or abnormal cancer cells express do not express self peptides in MHC class 1 and are therefore killed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

NK cells release granules from there cytoplasm. What do these contain and how do they kill infected cells?

A

Perforin and granzymes.

Perforin forms pores in the membrane of the target cell through which granzymes enter and induce apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How are NK cells activated?

A

In respose to interferons released from infective/cancer cell (direct activation) or by macrophage derived cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What do virally infected cells produce and release and how does this protect the immune system from viral spread?

A

Interferon alpha and beta

1) Signals unifected cells to destroy RNA and reduce protein synthesis
2) Signals infected cells to undergo apoptosis (reduces resovior)
3) Activates NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the systemic response of acute inflammation?

A

Change in plasma concentration of specific proteins due to altered protein synthesis in the liver. Driven by cytokines produced during the local inflammatory response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Give examples of pro-inflamatory mediators?

A

Histamine, leukotrienes, nitric acid, prostaglandins (and proinflamatory cytokines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the function of proinflamatory cytokines?

A

Stimulate the bone marrow to increase immune cell production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

CRP, SAP and compliment proteins are examples of acute phase proteins, what is the role of these molecules?

A

Prevent the spread of infection

*used as a diagnostic marker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Fibrinogen is an example of an acute phase protein, what is the role of this molecule?

A

Wound healing and coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

CRP, haptoglobin, manganese superoxide dismutase and protease inhibators are examples of acute phase proteins, what is the role of these molecules?

A

Prevent systemic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the local effects of acute inflammation?

A

Rubor, calor, tumor and dolor

Production of proinflamatory mediators, proinflamatory cytokines and chemokines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q 
What are the functions of:
a) Proinflamatory mediators
b) proinflamatory cytokines
c) chemokines 
as local effects of acute inflammation?
A

a) Proinflamatory mediators- vasodilators, ^vascular permeability, ^smooth muscle contraction and pain
b) proinflamatory cytokines- ^vascular permeability and endothilial cell activation
c) chemokines- leukocyte (neutrophil) recruitment and activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where does transendothilial migration take place?

A

Post capillary venuoles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe transendothilial migration for a neutrophil. Pro inflammatory cytokines and chemokines are released by macrophages and mast cells…

A

1) ^vascular permeability. Gap junctions are effected and endothilial cells contract making them leaky. Fluid is lost and viscosity increased at the endothilial layer => decreased blood flow and cell margination.
2) Vasodilation and increased blood flow to the site of infection
3) Endothilial cell activation. Activated endothilial cells express Selectins and ICAM proteins on their membrane
4) Neutrophils bind weakly to selectins using carbohydrate molecules (low affinity => selectin mediated rolling), Neutrophils bind strongly to VCAM/ICAM as they express integrins => stable adhesion and aggregation. Neurophils sqeeze between epithilial cells. DIAPEDESIS
5) Chemotaxis of neutrophils to the site of inflammation. due to chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Where do neutrophils reside?

A

Blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which cells lives longer, neutrophils or macrophages?

A

Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Histologically, how are neutrophils identified?

A

Intracellular granules and a multilobed nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the functions of neutrophils?

A

1) Kill extra cellular pathogens- recognition using PRR:PAMPs
2) Produce more pro-inflamatory cytokines which reinforce inflamation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the 3 mechanisms of killing by a neutrophil?

A

1) Phagocytosis
2) Degranulation
3) Neutrophil extracellular traps (NETs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Neutrophil phagocytosis: once encapsulated, neutrophils kill pathogens in 2 ways. What are these?

A

1) Antimicrobial proteins and enzymes

2) Reactive oxygen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How does a neutrophil phagocytose using antimicrobial proteins and enzymes?

A

1) Phagosome fuses with azurophilic and specific granules
2) pH rises and the antimicrobial response is activated and the bacterium killed
3) pH decreased and fusion with a lysozyme allows acidic hydrolyases to degrade the bacterium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How does a neutrophil [hagocytose using reactive oxygen species?

A

1) Assembly of the NADPH oxidase complex

2) production and release of ROS into phagosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How does a neutrophil kill by degranulation?

A

Release if antibacterial proteins from neutrophil granules into the extracellular environment
=> direct killing of extracellular killing of extracelluar bacteria and fungi
=> Tissue damage and potential systemic inflammation. This is non specific and can damage host tissue resulting in sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Neutrophil degranulation can damage host tissue resulting in sepsis. How is this response regulated?

A

Increased expression of protease inhibators (acute phase protein) by hepatocytes- try to limit damage to host cells.
Macrophages promote rear and healing following the infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How does a neutrophil kill by Neutrophil extracellular traps (NETs)?

A

1) Activated neutrophils release intracellular structures into the extra cellular environment. NETosis- neutrophils lyse their cell and nuclear membrane to commit suicide
2) NETs immobilise pathogens to prevent spread and this facilitates their phagocytosis.
NB: Proinflamatory cytocines are signaling the bone marrow to produce more neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the compliment system?

A

A family of 30 proteins produced in the liver and circulating in the blood. (10% of serum protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How is the compliment system activated?

A

Directly or indirectly by pathogens.

1) Classical pathway
2) Alternative pathway
3) Mannose binding lectin pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the functions of the complement system?

A

Pathogen killing
Pathogen opsinisation
Leukocyte recruitment and inflammation
Removal of immune complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How does the mannose binding lectin pathway work?

A

1) Cirtain bacterial species express mannose on their surface- mammals do not
2) MBL is an acute phase protein
3) When MBL binds to mannose on bacteria it causes cleaving of C3 to C3a and C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How does the alternative pathway work?

A

1) There is always a very low level of inactive C3 in the blood and over time it breaks down in the absence of an activator.
2) C3b is normally rapidly degraded but if it binds to a bacterial protein or carbohydrate, it is stabalised
3) C3b will then activate the amplification loop to cleave more C3 protein => activation of the compliment cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Human cells express proteins and carbohydrates which C3b can bind to but you do not want to activate the compliment system without a pathogen. How is this overcome?

A

Human cells have an inhibitory protein that will result in degradation of any bound C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How does the classical pathway work?

A

1) Activated by IgM and IgG binding to antigens.
2) This induces a confomational change in Ig mew and Ig gamma heavy chains which expose multiple binding sites for C1, the first component of the classical activation pathway.
NB: IgM is secreted as a planar structure but when bound to antigens becomes a crab like structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How does the compliment system kill pathogens?

A

Production of the membrane attack complex MAC

1) In the presence of C3b, C5 –> C5a + C5b
2) C5b generates MAC which creates pores in the pathogen membrane => osmotic lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How are encapsulated bacteria killed?

A

Activation of the complement system, production of MAC and osmotic lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is opsinisation?

A

Coating of pathogens by humoral factors (opsonins) to facilitate phagocytosis

68
Q

How does activation of the complement system lead to pathogen opsinisation?

A

C3b is an opsonin. (other eg. CRP, IgM and IgG)

69
Q

How does activation of the compliment system lead to leukocyte recruitment and inflammation?

A

1) C3a and C5a are anaphlatoxins and promote inflammation.
2) Act directly on blood vessels and activate mast cells which secrete proinflamatory mediators and chemokines
3) => ^permiability of blood vessels, fluid leakage and extravascularisation of immunoglobulini and complement molecules. TEM increases.

70
Q

Does compliment activation have an amplification loop?

A

Yes- using the alternative pathway

71
Q

What is an immune complex?

A

Antibodies cross linked with multiple antigens producing clumps

72
Q

The complement system is potent. How is it regulated?

A

Only cleaved compliment proteins are active
Active compliment proteins have a short half life
Some compliment proteins are only produced during an acute phase response
Some compliment proteins do not bind to human cells
Compliment inhibitors and regulatory proteins limit activation

73
Q

What characterises the adaptive immune response?

A

Slow and specific

74
Q

How is the adaptive immune system activated?

A

By antigens- any substance which can activate a T or B cell

75
Q

Each antigen has multiple epitopes. What does this mean?

A

Multiple T and B cells respond to the same antigen

76
Q

What is the main function of B cells?

A

Defence against extracellular pathogens by production of antibodies

77
Q

What is the main function of the 2 types of T cell?

A

CD4+ T cell = regulation of the immune response

CD8+ T cell (cytotoxic) = killing virally infected body cells

78
Q

Where are T cells produced and mature?

A

Produced in the bone marrow

Mature in the thymus gland

79
Q

Where are B cells produced and where do they mature?

A

Produced in the bone marrow and mature in the bone marrow

80
Q

Where do T and B cells reside in the body?

A

Constantly circulating in the blood, lymph and secondary lymphoid tissue. Inactive until they meet an antigen in secondary lymphiod tissue

81
Q

How many antigen receptors does each individual T and B cells express?

A

1

82
Q

What is a T cell antigen receptor (TCR)?

A

Membrane bound alpha beta heterodimer. 2 polypeptide chains creating a unique 3D shape

83
Q

What is a B cell antigen receptor (BCR)?

A

Membrane bound IgM or IgD (Y shaped antibody with flexible arms. 2 light and 2 heavy chains held by disulphide bonds)

84
Q

What are antibodies?

A

aka immunoglobulins
Proteins produced by B cells in response to a specific antigen. They are expressed on B cell surface and secreted as soluble proteins into the ECF.

85
Q

What is the structure of an antibody?

A

2 Ig heavy chains and 2 Ig light chains. Each has a variable and constant region.
Different types of antibodies exist with different Ig heavy chain constant regions.
The hypervariable regions of Ig light and heavy chains combine to form the antigen binding site
They are flexible

86
Q

The human genome only has 20000 protein coding genes so how can the adaptive immune system recognise millions of antigens?

A

Antibody heavy and light chains are coded for by segmental genes in the germ line genome of haematopoietic stem cells
Random arragement of these gene segments occurs in individual B cells as they develop.
Similar process for TCR alpha and beta chain segments

87
Q

Gene rearrangement is entirely random. Can autoreactive cells develop?

A

Yes

88
Q

How do T and B cells enter lymph nodes and where do they enter from?

A

Transendothilial migration from high endothilial venuoles

89
Q

What gets trapped in lymph nodes?

A

Dendritic cells, pathogens, antigens and debris

90
Q

What happens to T and B cells in the lymph node? Do they stay together?

A

Separate with the T cell zone in the central area and B cells are directed by chemokines to follicles around the centre

91
Q

If T and B cells do not encounter a pathogen in the lymph node, what happens?

A

Leave the lymph node via efferent lymphatics

92
Q

What are the 6 steps in which antigens can enter a lymph node?

A

1) Particles and antigens derived from a pathogen are released from phagocytosis
2) Inflammatory cytokines stimulate immature, tissue resident dendritic cells => expression of co-stimulatory molecules of dendritic cells.
3) Dendritic cells recognise and phagocytose pathogens and antigens using PAMPs:PRR
4) They digest the internalised pathogen derived antigens are display small paptides (7-10 amino acids) on there surface in complex with MHC class 2 proteins
5) Pathogen derived antigens and mature dendritic cells travel to locally draining lymph nodes
6) Enter by efferent lymphatics

93
Q

In healthy individuals where are dendritic cells, the communication between annate and adaptive immune system found?

A

Peripheral tissue (they are immature in healthy people)

94
Q

What is the function of dendritic cells?

A

Identify and phagocytose antigens, debris and particles (NOT whole cells)
Mature and migrate to secondary lymphoid tissue where they present antigens to T cells

95
Q

Give another name for MHC class proteins?

A

HLA proteins (human leukocyte antigens)

96
Q

How do T cells recognise pathogens?

A

Only recognise peptide antigens presented to TCR by MCH class molecules. They cannot recognise free antigens in lymph

97
Q

Where are MCH class 1 proteins expressed?

A

All nucleated cells

98
Q

What is the function of MHC class 1 proteins and how is this done?

A

Present peptide antigens to CD8+ T cells
If the cell is healthy, it will display a self peptide which is recognised by the TCR on CD8+ T cells => no response
If the cell is infected, it will present a peptide antigen from the pathogen, TCR will bind and activate CD8+ cells

99
Q

What is the function of MCH class 2 peptides?

A

Present peptide antigens from pathogens to CD4+ T cells

100
Q

Where are MCH class 2 proteins found?

A

Antigen presenting cells- dendritic cells ,macrophages and B cells

101
Q

T cell activation requires how many signals?

A

2

102
Q

What are the 2 signals required for T cell activation?

A

1) MCH peptide complex: TCR (partially activated)

2) Costimulatory molecules (B7): T cell surface protein (CD28) (Fully activated)

103
Q

Which cells express co stimulatory molecules if they encounter a pr inflammatory mediator?

A

Dendritic cells

104
Q

Where is a stromal cells found and what is its function?

A

Found in follicles in lymph nodes.

To increase chances of B cells encountering a pathogen

105
Q

What do stromal cells do?

A

Have Fc receptors which bind to opsonins
(Material released by phagocytosis stimulates CRP or C3=> compliment activation => opsonin production)
This makes it more likely the B cell will bind

106
Q

How many signals does B cell activation require?

A

2

107
Q

There are 3 pathways in which B cells are activated each with 2 signals. What are these pathways

A

1) Protein antigen
a) BCR: antigen
b) Tfh cell
2) Any antigen
a) BCR: antigen
b) PAMP: PRR
3) antigens with repetitive antigenic epitopes
a+b)multiple BCR : antigen engagement

108
Q

When is the “antigens with repetitive antigenic epitopes” activation of B cells important?

A

Encapsulated bacteria that contain repeated polypeptide chains in the capsule

109
Q

When B cells are activated, what happens and where?

A

Proliferate to produce many plasma cells in the follicle within the lymph node

110
Q

How does a plasma cell look different from an inactivated B cell?

A

Plasma cells are larger and have extensive ER for protein synthesis

111
Q

What type of plasma cells and antibodies are produced if B cells proliferate in the lymph folicle?

A

Short lived plasma cells that remain in lymph node (no memory cells)
Low affinity antibodies are secreted into the lymph and blood

112
Q

What type of plasma cells and antibodies are produced if B cells proliferate in a germinal centre?

A

Production of memory cells (with help from T fh cells)
Long lived plasma cells that produce and secrete high affinity antigens that migrate to the bone marrow where they live for decades secreting low levels of antigens.

113
Q

How is a germinal centre created?

A

Requires Tfh cells and => intense clonal expansion

114
Q

What are the 2 functions of antibodies?

A

Recognition: binding to antigen mediated by variable region
Effector: clearance mechanisms mediated by interactions of Ig heavy chain constant regions with effector molecules (complement or Fc receptors)

115
Q

What is the function of an Fc receptor?

A

To bind Ig heavy chain to an effector cell

116
Q

How many classes of antibodies?

A 
5
IgM (mew), IgG (gamma), IgD (delta), IgE (epsilon), IgA (alpha)
117
Q

Which antibody is secreted first and why?

A

IgM because the gene for the mew heavy chain is directly down stream of the gene for the variable region

118
Q

What are the 2 configurations of IgM and their functions?

A

1) Membrane bound monomer- B cell antigen receptor (BCR) used to activate B cells
2) Pentemer found in plasma
- Agglutination and immune complex formation
- Complement system activation via the classical pathway

119
Q

What is the most abundant antibody in human serum?

A

IgG (70-85%)

120
Q

Which immunoglobulin is produced in the highest quantities during a secondary/memory immune response?

A

IgG

121
Q

What are the 6 functions of IgG?

A

1) Agglutination and immune complex formation
2) Compliment activation via classical pathway
3) Foetal immune protection
4) Neutralisation
5) Opsinisation
6) NK cell activation

122
Q

What is foetal immune protection and how does this occur?

A

Where IgG antibodies are transported across the placenta directly into the foetal blood stream.
Ig gamma heavy chains have a high affinity for the Fc receptor gamma which is expressed in high concentrations in the placenta

123
Q

What is the function of neutralisation?

A

To neutralise pathogens preventing them entering host cells and prevents microbial toxins from disrupting host cells

124
Q

What mediates neutralisation and what are the high affinity neutralising antibodies?

A

Specific antigen binding

IgG and IgA dimeric

125
Q

What initiates and mediates opsinisation?

A

Initiated by specific antigen binding and mediated by Fc receptors that bind to opsinin (eg Ig gamma heavy chain)

126
Q

How does IgG activate NK cells?

A

Antibody dependent cell mediated cytotoxicity

1) Antigen specific IgG binds to infected cell
2) Ig gamma heavy chain binds to Fc gamma receptor on NK cells => activation

127
Q

What is the function of IgD?

A

B cell antigen receptor as a membrane bound monomer

128
Q

What is the second most abundant Ig type?

A

IgA

129
Q

What are the 2 forms of IgA?

A

1) B cell activation as a monomer present in SERUM

2) Secretory IgA as a dimer present in secretory fluid

130
Q

What are the functions of sIgA?

A

1) Neonatal defence as its present in colostrum and breast milk
2) Neutralisation at mucosal tissue

131
Q

What does IgE characterise and why?

A

ALLERGY
Fe epsilon receptors are present on mast cells and basophils.
When Ig epsilon heavy chain bound to antigen binds to Fe epsilon => degranulation

132
Q

How are antibodies of the same specificity but different Ig classes produced?

A

During B cell activation, B cells can switch the Ig heavy chain constant region gene segment in use by alternate mRNA splicing. They retain the same hypervariable region.
Process induced by cytokines

133
Q

When activated CD4+ T cells divide to produce T helper cells which regulate the immune system. Different T helper cells are produced by different cytokines. What re the 5 types of T helper cells and what are their functions?

A 
Th1 = killing of intracellular bacteria
Th2 = killing of helminths, worms, paracites (allergy)
Tfh = B cell co-stimulation
Th17 = killing of extracellular pathogens 
Treg = lymphocyte suppression
134
Q

Which cytokine does CD4+ secrete which causes proliferation of T helper cells?

A

Interleukin 2

135
Q

T helper cells also secrete IL 2 into the extracellular fluid. What does this stimulate?

A

Proliferation of CD8+ T cells

136
Q

Which immune cells do Th1 cells work with and how does this happen?

A

Macrophages

1) Th1 cells migrate from SLT into infected tissue sites
2) Th1 cells are reactivated by tissue resident macrophages in an antigen specific way (TCR:MHC class 2 peptide)
3) Th1 cells express co-stimulatory molecules (IFN alpha) that hyperactivity macrophages (ROS/RNS produced and more cytokines released)

137
Q

Which immune cells do Tfh cells work with and why?

A

B cells to help them respond to protein antigens (second signal)

138
Q

How do Tfh cells help B cells to respond to protein antigens?

A

1) Protein antigens bound to BCR are internalised by B cell and sntigen degraded and presented on B cell surface by MHC class 2
2) Effector Tfh cells move into the B cell follicle in the lymph node where they are restimulated by B cells in an antigen specific mannor (MHC:TCR) => expression of co-stimulatory molecules on Tfh cells
3) Re-activated Tfh cells secrete cytokines that further activate B cell and stimulate formation of a germinal centre

139
Q

What is the germinal centre response?

A 
B cell proliferation 
Differentiation into plasma cells
Differentiation into memory cells 
Ig heavy chain class switching 
Generation of high affinity antibodies
140
Q

When activated by T helper cells (releasing IL2) CD8+ T cells are activated- what do they divide to produce?

A

Cytotoxic T lymphocytes which kill infected host cells by migrating into the tissue

141
Q

What are the functions of effector cytotoxic T lymphocytes?

A

1) Recognise and bind to virally infected cells (MHC class 1 with viral peptide antigen)
2) Programmes target for death producing DNA fragmentation => Target cell dies by apoptosis

142
Q

How do cytotoxic T lymphocytes (and NK cells) kill infected host cells?

A

1) Release granules:
a) Perforin polymerises to from a pore in the membrane
b) Granzymes are serine proteases with activate apoptosis in the cytoplasm of a cell
c) Granulysin induces apoptosis
2) Fas ligand mediated killing. Fas ligand on CTL binds to Fas receptor on target cell which activates interleukin 1 beta converting enzyme => DNA fragmentation and apoptosis

143
Q

How do CTL kill by Fas ligand killing?

A

1) Fas ligand on CTL binds to Fas receptor on target cell 2) Activates interleukin 1 beta converting enzyme => DNA fragmentation and apoptosis

144
Q

3 reasons to vaccinate?

A

1) Effective at reducing/preventing disease
2) Critain pathogens are life threatening/altering
3) After clean water, vaccination is the most effective public health intervention in the world

145
Q

What is vaccination?
Why do we do it?
How does it work?

A

Deliberate exposure to an antigen
To induce immunolocically mediated resistance to disease
By inducing immunological memory (Long lived T and B cells to reduce the lag phase)

146
Q

If you have memory T and B cells for a pathogen how does this prevent disease?

A

Pre-existing IgG antibodies will clear the infection during the incubation period

  • IgG neutralises bacteria and toxins
  • Rapid mobilisation of phagocytes + complement
  • Pre-formed sIgA blocks bacterial attachment to mucus membrane
147
Q

What is immunisation?

A

The process through which an individual develops immunity to a disease (inc. deliberate and natural infection)

148
Q

What is vaccination?

A

Deliberate administration of antigenic material to produce immunity to a disease

149
Q

What is active immunity?

A

Protection produced by the individuals own immune system which is usually permanent. Stimulated by natural infection or vaccine

150
Q

What is passive immunity and give 2 examples?

A

Protection transferred from another person or animal. Temporary protection which wains with time
Breast feeding or rabies shot

151
Q

How does vaccination lead to production of memory T and B cells?

A

1) Vaccination stimulates nieve T and B cells to induce an adaptive immune response within 14-21 days.
2) Some become effector cells which mostly die by apoptosis is absence of persisting antigen
3) Smaller number become memory cells and are maintained at a lower frequency

152
Q

What are the advantages of having memory CD8+, CD4+ T cells and memory B cells?

A

Memory CD8+ T cells kill immediately on antigen stimulation
Memory CD4+ T cells produce cytokines immediately on antigen stimulation
Memory B cells have already undergone Ig class switching.
All have enhanced cell adhesion and chemo taxis

153
Q

What are the types of active vaccination?

A

Infectious organism (natural)
Live attenuated
Inactive - Killed, subunit or toxiod

154
Q

What is a live attenuated vaccine?

A

Exposure to the same but a less virulent pathogen

155
Q

What is an inactive vaccine?

A

Exposure to an inactivated, part of pathogen or product of the pathogen. (Generally not as effective)

156
Q

Why are inactive vaccines less effective than live attenuated vaccines?

A

Cannot replicate and the immune response is mostly antibody based (not T cell)
Antibody titre can diminish over time
Often require multiple doses to stimulate an immune response

157
Q

How is an inactive vaccine produced?

A

Exppose the pathogen to heat, chemicals or radiation

158
Q

What are the advantages of inactive vaccines?

A

+ made quickly to prevent epidemics.
+ good antibody response
+ easy to store- no refrigeration required
+ usually safe and can be given to immunocomprimised

159
Q

What are the disadvantages of inactive vaccines?

A
  • Under (still toxic) or over (loss of antigenicity) inactivation
  • Multiple doses required to generate memory cells
  • Poor T cell response
  • Hard to stimulate immune system
160
Q

What is a adjuvant?

A

Mixture of inflammatory substances required to stimulate immune responses to co-administered peptides, proteins or carbohydrates.
Added to vaccinations

161
Q

Give 3 examples of adjuvants?

A

Aluminium hydroxide
Toxins- tetanus toxiod
Other pathogens

162
Q

Why are adjuvants added to vaccinations?

A

Create an inflammatory environment to stimulate an active immune response.
But can be toxic and can lead to immune system responding to adjuvant rather than vaccine

163
Q

What are the advantages of live attenuated vaccines?

A

+ Similar to natural infections
+ Localised strong response of antibodies and T cells
+ Usually one dose required

164
Q

What are the disadvantages of live attenuated vaccines?

A
  • Must replicate to be effective
  • Safety- may acquire new mutations and revert to virulence causing infection esp. immunocomprimised
  • Fragile and may need refridgeration
165
Q

How is a baby protected from infection by passive immunity?

A

1) Active transport of maternal IgG across the placenta in 3rd trimester
2) IgA in breast milk and colosterum which is important for colonisaiton of the GI tract
* exposure to infection while protected by maternal antibody may result in less severe infection but will still produce memory

166
Q

What is therapeutic passive immunisation?

A

Transfer of an antibody from an unrelated individual.

Pooled normal immunoglobulin form and immune individual

167
Q

What is Hyper immune Globulin?

A

Immunoglobulin from individuals knwon to have high antibody levels against a specific pathogen.
Administered after specific exposure eg rabies and antivenom

Principles (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions