Brainscape's Knowledge GenomeTM

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


See full index

PHAY00011 > Immunology I > Flashcards

Immunology I Flashcards

1
Q

What are the three primary levels of defence of the immune system?

A

1/ External barriers
2/ Innate immunity
3/ Adaptive immunity

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

What are the main differences between the innate and the adaptive immunity? <Hint: 6 differences>

A

1/ Complements - Antibodies
2/ Broad specificity - High specificity
3/ Chiefly disposal - Mainly recognition
4/ Rapid - Slow
5/ No memory - Memory cells
6/ Both invertebrates and vertebrates - Only vertebrates

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

The three key features of the immune system:

A
  1. Ability to recognise pathogens AND differentiate non-self
  2. Mechanisms to kill or to eliminate the pathogens
  3. Method of coordinating the activities by the use of signalling molecules called cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define cytokines and give examples

A

LMW proteins

Cellular growth, differentiation and inflammation and repair

Examples: IL, IF, TNF, colony-stimulating factors, chemokines

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

How are non-self cells recognised by innate immunity?

A

Pattern recognition receptors (PPRs)

Identify PAMP (pathogen-associated molecular patterns) - common antigens

PPRs: both cell surface and cytoplasm

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

4 main types of PAMPs

A

Nucleic acid - ssRNA, dsRNA (virus)

Proteins - pilin, flagellin (bacteria)

Cell wall lipids - LPS (gram-negative), lipoteichoic acid (gram-positive bacteria)

Carbonhydrates - Mannan, Dectin glucans (fungi and bacteria)

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

How does the body recognise previously non-encountered pathogens?

A

Through TCRs and BCRs

Highly specific

Target: peptides present on MHC (major histocompatibility complex) molecules

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

Compare the receptor variation between innate and adaptive

A

Innate: not varied system of receptors. Same type of cells = same types of receptors.

Adaptive: each cell contains unique receptors

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

Primary lymphoid organs

A

Lymphocyte formation, development and maturation

Bone marrow and thymus

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

Secondary lymphoid organs

A

Recognising and responding to foreign materials

Lymph nodes (tonsil etc), spleen, Peyer’s patches

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

Lymphatic system and infection

A

Antigens captured - enter lymphatic system -> regional lymph nodes

Lymphocytes will parade to the infected areas from the lymph nodes

Adhesion molecules + chemokines attract lymphocytes to infected tissues

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

Recirculation of lymphoid system

A

Constant flow of lymphocytes from blood -> tissue -> lymph -> blood

Allow lymphocytes to make contact with antigen no matter its location

Neutrophils enter infected tissues, not return

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

Composition of innate immunity

A

Physicochemcial or biochemical factors/barriers

Humoral system

Cellular system

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

Physicochemical factors of innate immunity include:

A

Mechanical barriers - keratinised epithelium of skin

Antimicrobial enzymes

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

Antimicrobial substances produced by innate immunity

A

Lysozyme: hydrolyses peptidoglycan

Phospholipase A2: destroy bacterial membrane

Defensins: cationic peptides, form pors on bacterial membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does Innate system cause inflammatory response?

A

Activation of complements

Activation and attraction of phagocytic cells - cytokine releases

Activation of natural killer cells

Altering the vascular permeability

Increasing body temp (cytokine effects)

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

4 main characteristics of inflammation

A
  1. Pain: dilation - tissue - pain receptors
  2. Heat: dilation - movement of cytokines
  3. Redness: blood accummulation
  4. Swelling: fluid accummulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Definition of complements

A

Soluble humoral factors

Bring about the lysis of the bacteria

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

Roles of complements in inflammation and immunity

A

Chemotaxis of phagocytes

Activate mast cells

Opsonisation and cell lysis

Immune complex clearance

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

Three activation pathways of complements

A

Classical pathway: complement - antibodies -> activation + cascade reaction -> lysis

Lectin pathway: complement - sugar complex -> activation + cascade reaction -> lysis

Alternative pathway: complement - direct binding to surface

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

Complement recognition in Classical pathways

A

C1qrs - antibodies on microbe

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

Mechanism of activation - Classical Pathways

A

C1qrs bind to antibodies -> conformational change -> C4 bind + C1qrs activated C1r2s2 (serine protease) -> C1r2s2 cleaves C4 into C4b -> C4b bind to Ab -> C2 bind to C4b, get cleaved to 2b -> 2b bind -> C4b2b (C3 convertase)

C4b2b cleaves C3 into C3a + C3b

C3b involved cleaving C5 into C5a + C5b

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

General mechanism of activation of complement activation pathways

A

Recognition and binding

Conformational changes -> activation of serine protease

Hydrolysis of the next component in cascade

Binding, further conformational changes

More serine protease activation

Repeats until C3 convertase produced

C3 convertase -> C3a (inflammatory response) and C3b (cell lysis, phagocytosis and immune complex clearance)

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

General roles of C3a, C3b, C5a and C5b in immune response

A

C3a -> inflammation
C3b -> opsonisation and phagocytosis
C5a -> inflammation
C5b -> lysis of bacteria (MAC)

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

Complement recognition in Lectin pathways

A

Mannose-binding lectin (MBL) - mannose

Ficolin - N-acetylglucosamine

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

C1 inhibitors definition and mechanism of action

A

Plasma serine protease inhibitor controlling the classical and lectin pathways

remove the C1r and C1s from the complex -> no enzyme C1r2s2 -> no classical pathways

remove MASP-2 from MBL or ficolin -> no lectin pathway

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

Mechanism of activation - Lectin pathways

A

MBL (collectins) interact with mannose -> activation and complexing with MASP-1 and MASP-2 -> C4 and C2 is cleaved into C4b and 2b -> Formation of C4b2b (C3 convertase)

C4b2b cleaves C3 into C3a + C3b

C3b involved cleaving C5 into C5a + C5b

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

Mechanism of activation - alternate pathways

A

Spontaneous activation of C3 -> C3b

Normally inactivated by hydrolysis, but in infection + Mg2+ ions present -> bind to surface -> no inactivation

C3b + factor B -> C3bB complex

Factor D cleaves factor B into Ba (leave) + Bb (bind to form C3bBb = C3 convertase)

Factor P (properdin) stabilises C3bBb

Another C3b binds to C3bBb to form C5 covertase

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

Regulation of alternate pathways

A

Factor I and factor H in plasma: cleave C3b -> iC3b

Membrane cofactor protein (MCP): cleave C3b -> iC3b

Complement receptor 1: cleave C3b -> iC3b

Decay accelerating factors (DAF): displacement Bb -> no C3bBb

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

Membrane attack complex (MAC). Definition and formation.

A

C5 convertase (from C3b) -> C5b fragment

C5b combine with C6,C7,C8 -> MAC form

MAC makes holes in bacterial membrane -> lysis

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

How are host cells protected from MAC?

A

CD59 protein on the cell membrane -> prevent insertion of C9 proteins (pore forming agents) -> no MAC

Fluid phase regulator S protein -> interfere insertion of C5b - C7 complex -> no MAC

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

Explain the biological activities of complement activation <Hint: 5 points>

A
  1. MAC formation -> bacteria osmotic lysis (C5 covertase)
  2. Opsonisation -> stimulate neutrophillic removal
  3. Opsonisation -> C3b receptor recognition -> phagocytosis
  4. Recruitment and activation of cells and promote inflammation (C4a, C3a and C5)
  5. Removal of immune complexes (C3b) -> maintain small + attach to Erythrocyte CR-1 -> removal by liver and spleen via resident macrophage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does activation of PPR upon binding to PAMPs lead to?

A

Dimerisation of 2 receptors

Binding of adaptor molecules like Myd88 and TRIF -> stimulate signalling pathways

Gene activation
Pro-inflammatory cytokine production
Stimulation of adaptive immunity
Interferon production

Dependent on type of activated receptors + cross-talk between diff sginalling pathways

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

How are macrophages activated?

A

Microbial products

IFN-gama released from NK cells

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

The proteins produced by activated macrophages

A

Phagocyte oxidase: produce reacive oxygen species -> kill

iNOS - produce nitric oxide -> kill

Cytokines like TNF, IL-1, IL-12: inflammatory response + enhance adaptive immunity

Fibrolast growth factor: tissue remodelling
Angiogenic factor: tissue remodelling
Metalloproteinases: tissue remodelling

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

Activity of IL -1

A

Act on: vascular endothelium

Increased permeability
Stimulate production of IL-6

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

Activity of IL-6

A

Act on: Liver

Produce acute phase proteins like CRP
Elevate body temperature

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

Activity of IL-8

A

Act on: vascular endothelium

Activate vascular endothelium
Attract and activate neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Activity of IL-12

A

Act on: NK cells

Activate NK cells
Influence lymphocyte differentiation

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

Activity of TNF-alpha

A

Act on: vascular endothelium

Increased permeability
Activate vascular endothelium

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

How do cytokines exert their effects locally and systemically?

A

Local inflammation - production of adhesion molecules + increase in permeability of cells -> allow innate immunity cells to enter tissue

Local effects - trigger production of more cytokines molecules

Systemic effects - protective effects and pathological effects

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

Examples of how cytokines involved in protective systemic effects

A

TNF, IL-1, IL-6 - brain - fever

IL-1, IL-6 - liver - acute phase proteins labelling the microorganism.

TNF, IL-1, IL-6 - bone marrow - lymphocyte productions

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

Examples of how cytokines involved in pathological effects

A

TNF - heart - increased heart rate

TNF - endothelial cells + blood vessels - increased permeability

TNF - insulin resistance in many tissues

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

Name and describe some examples of phagocytic cells

A

PMN - phagocytosis and killing of bacteria and fungi

Monocyte - Precursor of macrophage

Macrophage - phagocytosis

Kupffer cells - Major phagocyte in liver - clear blood

Mesangial cells - phagocyte in renal glomerulus - remove complexes

Microglial cells - phagocyte in brain

Dendritic cells - APC of lymphoid tissue

Langerhans cell - dendritic cell of skin

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

Neutrophils - definition

A

Produced in bone marrow

PMN leukocytes, granulated cells

Many types of receptors on the surface

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

What are the different types of receptors present on the surface of neutrophils?

A

Recognise PAMPs

Recognise antibodies

Recognise complement components

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

Neutrophils - margination

A

Neutrophils rolling along the margin of blood vessels

Allow to stop at site of infection and pass into tissues

Via weak interaction between the selectin ligands on neutrophils and the glycoprotein on endothelial cells

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

Neutrophils - Entering the damaged tissue

A

Mediators attracting neutrophlls are released

Endothelium respond to distress signal -> release intracellular adhesion molecules (ICAMs)

ICAMs induce tighter binding of neutrophils to cells in damage regions

Chemotaxins - neutrophil cross junction (diapedesis)

Migrate towards site of infection down chemotactic gradients (chemotaxis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Potent chemotactic factors

A

Complement C5a

Chemokine IL-8 released from damage tissue

Bacterial cell wall products like N-formylated peptide

LTB4, a leukotriene pro-inflammatory mediator released by neutrophils

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

Neutrophil - chemotaxis

A

Chemostatic factors bind to receptors on the edge

Pseudopodium formation (foot-like extension) -> movement

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

Neutrophil - phagocytosis

A

Approach the bacteria - engulf (phagocytosis)

Ineffective without co-factors and opsonins coating the surface

Opsonin bind to neutrophil receptor -> pseudopodia formation -> engulf -> localise within phagosome

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

Name highly effective opsonins

A

Complement components

C-reactive proteins

Antibodies

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

Neutrophil - killing mechanism

A

Oxygen independent

Oxygen dependent

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

Neutrophil - oyxgen-independent mechanism

A

Lysozyme: hydrolyse cell wall

Lactoferrin: iron-binding protein -> reduce irons available

Defensins: direct insert -> damage membranes

Phospholipase A2: enzymatic activity -> damage membrane

Can act synergistically (BPI and phospholipase A2)

Important in highly anaerobic conditions like deep abscesses

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

Neutrophil - oxygen-dependent mechanism

A

Complex - involve several radical and chemical species

Hydrogen-peroxide-myeloperoxidase-halide system:
+ NADPH oxidase reduces O2 to superoxide
+ generation of H2O2 (bactericidal)
+ myeloperoxidase use H2O2 covert Cl- -> highly toxic hypochlorous ions

Respiratory burst:
+ Superoxide anion is produced
+ H2O2 is produced
+ hydroxyl radicals is produced.

51
Q

How do neutrophils protect themselves from the reactive substacnes?

A

Antioxidants

Scavenging molecules like vitC and vit E

52
Q

Mast cells - Roles

A

Skin, around blood vessels and gut

Important for acute inflammatory response

Granulated: histamine, leukotrienes -> increased vascular permeability -> migration of fluid and chemicals to infection site + diapedesis

Receptors for IgE, C3a, C5a -> if bind, degranulation

53
Q

Basophils - roles

A

Found in blood

Important for acute inflammatory response

Granulated: histamine, leukotrienes -> increased vascular permeability -> migration of fluid and chemicals to infection site + diapedesis

Receptors for IgE, C3a, C5a -> if bind, degranulation

54
Q

How does anaphylatic shock occur?

A

Vasodilation occurs throughout the body uncontrollably

55
Q

Effects of prostagladins released from mast cells

A

Vasodilation
Bronchoconstriction
Headache

56
Q

Effects of leukotrienes released from mast cells

A

Bronchoconstriction
Asthma symptoms
Build up of mucus -> airway obstruction

57
Q

Effects of histamin, bradykinin and serotonin on smooth muscle

A

vasodilation -> redness + itch
bronchoconstriction
increased peristalsis of intestine -> V + diarrhoea

57
Q

Effects of histamins, bradykinin and serotonin on secretory glands

A

Excessive mucus
Tear formation

58
Q

Dendritic cells - roles in the body

A

Low in blood, high in tissues

Migrate from peripheral tissues to secondary lymphoid

PRRs on surface

Antigens, peptides of pathogen presented on MHC II complex -> show to activate antigen specific T cells -> adaptive immune

59
Q

Natural killer cells - roles in the body

A

Large granular lymphocytes

Cytotoxtic

Kill tumour cells, virus infected cells

60
Q

Natural killer cells - activation mechanism

A

Activator receptors (ARs) - recognise glycoproteins on various cell types

Inhibitory receptors - recognise the MHC class I receptors on host cells

61
Q

Natural killer cells - killing mechanism

A

Release of lytic enzymes: perforin and granzymes

High Ca2+ -> perforin insert to membrane -> increased permeability

Granzymes enter -> cleave and activate intracellular capases -> apoptosis

Produce IFN-gama -> macrophages activation + growth inhibition

62
Q

What stimulates IFN-gama?

A

IFN-alpha, IFN-beta released from phagocytes

TNF, IL-12, IL-18 released from phagocytes

63
Q

IFN-alpha and IFN-beta other effect beside stimulate IFN-gama production?

A

Induce resistance to viral infection of uninfected cells

Via Type 1 IFN receptors

64
Q

Tissue monitoring in adaptive immunity

A

Blood monitoring -> spleen

Solid organs and peripheral tissues monitoring -> lymph nodes

Intestine -> Peyer’s patches (additional)

Naive lymphocytes circulating around the body

65
Q

How are lymphocytes different from other immunological cells?

A

Recirculate through blood, tissues and lymphoid organs

Individually specific

Recognition -> proliferating + respond thru secretion or cytotoxicity

Can remain as memory -> larger response if encounter again

66
Q

Where are B cells produced?

A

Bone marrow

67
Q

Where are T cells produced?

A

Thymus

68
Q

Compare differences between B cells and T cells.

Surface markers?
Circulation in blood?
Receptors for antigens?
Distribution in lymphoid?
Require MHC-antigen complex?
Events upon antigen stimulation?
Function?

A

Surface markers: Ig - TCR + CD molecules

Circulation in blood: low number - high number

Receptors for antigens: BCRs - TCRs

Distribution in lymphoid: cortex - paracortical sites

Required MHC-antigen complex: No - Yes

Antigen stimulation: Plasma cells/memory cells - several types/memory cells

General function: Produce Ig - Helping other immune cells/ killing abnormal cells/ cytokines release/ hypersensitivity

69
Q

What happen to B cells upon recognition to antigens?

A

Differentation into plasma cells that can synthesise antibodies

Produce BCRs (similar to the antibodies produced)

70
Q

Do BCRs have any intrinsic enzymatic activities?

A

No - only for recognition purpose

Cannot direclty signal the cells to produce antibodies

71
Q

How are B cells activated upon BCRs binding to antigen?

A

Not activated immediately

Require other co-stimulatory binding such as C3b and the complement receptors on the B cell surface.

72
Q

How are diversity of the BCRs achieved?

A

Gene random recombination process:

Different genes combine together through the activity of recombination activating genes
-> Wide range of BCRs

73
Q

Explain the mechanism preventing generated BCRs recognising autoantigen.

A

Eliminating mechanism

Newly generated B cells - screen -> if recognised autoantiegn - apoptosis, if not - enter the blood

74
Q

Where are B cells and T cells resident in the lymph nodes?

A

Primary follicles (subcapsule): macrophages and B cells

Secondary follicles (germinal center): Activated B cells and few T helper cells

Medulla: macrophages and T cells

75
Q

What are the two routes of B cells activation?

A

T cell-independent antigens activating B cells

T cell-dependent process

76
Q

Describe the T-cell independent activation process of B cells.

A

Antigens with intrinsic mitogenic activity like LPS - induce B cells -> plasma cells

Antigens with repeated identical antigenic determinants

Example: polysaccharides found in Meningococcus, Haemophilus, Strep.pneumoniae

77
Q

What are the limitations of B cells activated by T-cell independent process?

A

Restricted to IgM production

No memory cells produced

78
Q

Describe the T-cell dependent activation process of B cells.

A

B cells present antigen on MHC class II

Activated T helper cell (by dendritic cells presenting the same antigen) recognise the complex -> produce cytokines

Induce clonal expansion + differentiation into plasma cells -> antibodies AND memory cells

79
Q

Describe the structure of an antibody.

A

2 identical long heavy chains + 2 identical short light chains

Random recombination process to generate each chain

Y-shape: variable antigen binding at tips + constant stem

Hinge region - for binding of spaced antigens if needed

80
Q

Different classes of antibody

A

IgM, IgG, IgA, IgE and IgD

81
Q

Explain the properties and function of IgM

A

First Ig produced in primary immunity

Produced in T-cell independent process

Neutralising, immobilising, prevent adherence, agglutinate

Activate classical pathway of complement activation

82
Q

Explain the properties and function of IgG

A

Longest term of protection

Can cross placenta

Neutralising, immobilising, prevent adherence, agglutinate

Induce phagocytosis,

Activate classical pathway

Elicit ADCC

83
Q

Explain the properties and function of IgA

A

Stable against hydrolysis -> immunity in mucosa

Found in breast milk - protect infant GI

Neutralising, immobilising, preventing adherence

84
Q

Explain the properties and function of IgD

A

Involved in development and maturation of Ig response

Unclear function

85
Q

Explain the properties and function of IgE

A

Fc region bind to mast cells + basophils

Degranulation

Allergic reaction

86
Q

Explain how the diversity of antibodies can be achieved.

A

A large number of genes for variable regions, joinging regions, constant regions and diversity

Random recombination

87
Q

What are the 3 types of antigens?

A

Endogenous antigens

Exogenous antigens

Autoantigens

88
Q

What is epitope? What is it structure

A

Antigenic determinants - region specifically recognised by antibodies

Small part of V domain, coded by V gene - 3D structure

6 hypervariable loops, 3 of light chains + 3 of heavy chains

89
Q

What is the different between affinity and avidity?

A

Affinity is the strength of binding between recognition site and one epitope

Avidity is strength of antibody binding to ALL sites

90
Q

What are the functions of antibodies?

A

Agglutination - reduce total number of infectious units

Activation of complements - thru Fc domain binding

Opsonisation - label for phagocytosis

ADCC - Fc domains activate macrophages, eosinophils + NK cells

Neutralisation - block adhesion and attachment

91
Q

Compare primary and secondary response

A

Secondary more rapid

Secondary longer duration

Secondary larger respond

Secondary mainly IgG, some IgM. Primary mainly IgM, later switch to IgM|G

Secondary higher affinity

92
Q

Why does IgG have longer half-life?

A

Binding to neonatal Fc receptors (FcRn) on endothelial cells

Pinocytosis -> endosome fusion -> conformation changes due to lower pH -> bind -> signal to release backout

Repeat multiple times along -> avoid clearance process

93
Q

What is used to treat chronic inflammatory allergic reaction?

A

IV IgG - saturate FcRn - induce lysosome degradation of IgG

94
Q

How can IgG is the only antibody can cross the placenta?

A

By interaction with FcRn

95
Q

What cells are responsible for rapid and stronger antibodies response upon re-infection?

A

Memory B cells

96
Q

How can memory B cells mount a more rapid and stronger antibodies response?

A

More specific antibodies

More rapid differentiation into plasma cells

Remaining of IgA and IgG switched from IgM from primary response

High frequency of somatic mutation -> selection of cells with highest affinity

97
Q

What mediate the switch from IgM to other types of antibodies?

A

Mediation of T helper cells

Presence of cytokines:
- IFN-gama -> IgG
- IL-4 -> IgA
- TGF-beta, APRIL, BAFF -> IgA

98
Q

What happened to naive T cells upon recognition?

A

Differentiate into:
- T helper cells -> activate other immune cells
- Cytotoxic T cells -> combat infected host cells
- Memory T cells

99
Q

What are activation of T cells dependent on?

A

The recognition of TCRs with the pathogenic peptide- MHC complex molecules

100
Q

What are the two class of MHC molecules?

A

Class I MHC = all nucleated cells - determination of self - present peptides from proteins within the cells

Class II MHC = only on APCs like macrophages, dendritic cells, B cells - present to T cells - activate T cells or being activated by T cells

101
Q

What are the two pathways that antigen display via MHC molecule take place?

A

Endogenous pathway - MHC class I - in most cells

Exogenous pathway - MHC class II - APCs only

102
Q

Describe the endogenous pathways of MHC display.

A

Cells are already infected

Proteasomes chop the proteins (both host can pathogen) -> peptides

Peptide delivered to RER by TAP (transport protein)

MHC class I - peptide complez formed

Golgi-dervied vesicles deliver to the surface

103
Q

Describe the exogenous pathways of MHC display

A

Pathogen phagocytosed by APCs

Acid and proteases cleave pathogen protein -> peptide.

MHC class II made in RER, binding groove still blocked by invariant chain

MHC class II transported to phagolysosome by vesicles

Fusion -> invariant chain exchanged with peptide -> complex form

Complex moved to surface

104
Q

Compare and constrast TCRs and BCRs

Recombination of V-J-C genes?
Junctional delivery?
Subsequent mutation?
Chain structure?
Recognition target?
Secreted in blood?

A

The genes for TCRs are only in T cells, same for BCRs and B cells.

Both have junctional diversity

Only BCR has subsequent mutation

TCR (alpha+beta OR gama + delta) while BCR (2 heavy from M,G,D,A or E + 2 light from lamda and kappa)

TCRs target small linear molecule on MHC and Glycolipid and CD1 ligand. BCRs target 3-D shapes of proteins or sugar

Only BCRs can be secreted in blood, TCRs are bound to surface permanently

104
Q

How can diffrent types of T cells respond to correct target cells?

A

Through the surface molecules, especially the MHC-peptide complex.

CTLs - CD8 molecules recognise MHC I complex

T helper cells - CD4 molecules recognise MHC II complex

105
Q

How can TCRs be prevented from recognising autoantigen?

A

Being screened twice

First - Thymus - if recognise MHC I complex - yes, progress - no, apoptosis.

Second - if recognise MHC - autoantigen complex - yes, apoptosis, or Regulatory T cells - no,progress ready for action

106
Q

Why can T cells only recognise peptides and no other molecules?

A

Only peptide can bind to MHC complex molecules

TCRs only recognise the MHC-peptide molecules.

107
Q

Why do T cells only recognise linear peptides, not 3-D like B cells?

A

Protein conformation is lost during the generation of the peptides that can bind to the clefts of the MHC moleculesWhy

108
Q

Why do T cells only recognise cell-associated antigens only, not soluble free antigens?

A

TCRs can only recognise MHC-like shapes with peptide attached on it

MHC is a membrane bound

109
Q

Why do CD4+ cells and CD8+ cells recognise antigens from the extracellular pools and cytosolic pools respectively preferentially?

A

Each pool undergoes different antigen presenting pathways (endogenous + exogenous)

CD4 bind to MHC class II
CD8 bind to MHC class I

110
Q

What determines the subtypes of T helper cells that T cell differentiates into? Give example

A

Dependent on signalling molecules.

IFN-gama -> T helper-1 cells

IL-4 -> T helper-2 cells

IL-17 -> T helper-17 cells

111
Q

Roles of T helper-1 cells.

A

Cell-mediated immunity

Control of intracellular pathogens

Delayed hypersenstivity

Macrophage stimulation

112
Q

Roles of T-helper-2 cells

A

Activation of B cells

Activation of mast cells and basophils

Activation of eosinophils - control extracellular parasites

113
Q

Roles of T-helper-17 cells

A

Recruitment and activation of neutrophils - important for control against bacteria and fungi

114
Q

Describe the activation and recruitment of cells in lymph nodes

A

In secondary lymphoid tissues

Antigens arrived from: acquired DCs or soluble free

Soluble free antigens can be acquired from resident DCs at T cell areas. Some activate B cells

DCs recruit lymphocytes from naive B cells and T cells constantly circulating -> if recognise, retained in node and activated - if not recognise, leave the node

115
Q

What are the requirements for T cell activation at lymph nodes?

A

Interactions between TCRs and MHC-peptide complex

Co-stimulatory non-antigen specific interaction:
B7 (APC) and CD28 (T cells)
CD40 receptors (APC) and CD40 ligands (T cells) - expression from MHC-TCR interactions

Released cytokines from activated APCs

116
Q

What is the general effect of CD40 ligand expression?

A

Promote and amplify T cell activation via interaction with cytokines and their receptors

117
Q

Once activated in the lymph nodes, what do T helper cells do?

A

To B cell follicles to activate B cells -> antibodies

Remain -> activate CD8 T cells (Cytotoxic T cells)

Leave lymph node -> blood -> peripheral site -> activate different immune cells

118
Q

What are the interactions between T helper cells and macrophages?

A

IFN-gama released from T helper cells

CD28 - B7
CD4 - MHC class II peptide complex
CD40L - CD40

119
Q

What happen after T helper cells activate macrophages?

A

Activated macrophages - killing mechanism (oxidative - non oxidative) thru production of reactive oxygen species, nitric oxygen, lysomal enzyme

Secretion of cytokines and chemokines - recruit leukocytes (esp IL-12 induce more differentiation of T helper cells and trigger IFN-gamma production)

Increased expression of B7 and MHC molecules on surface - amplife T cell response

120
Q

The roles of cytokines between CD4 T cells and macrophage

A

Mutally activate each other

CD4 T cells release cytokines - activate recruited leukocytes

Down regulate the response - by causing death and suppression of T cells

121
Q

How is cytotoxic T cell activated?

A

By APCs and T helper cells

Via recognition of peptides bound to MHC class I molecules

122
Q

Function of cytotoxic T cells

A

Secrete IFN-gamma and TNF

Promote cell deaths to target infected cells via 2 pathways

123
Q

What are the two pathways through which cytotoxic T cell promote cell death?

A

Pathway 1: Release of cytotoxic agent
Perforin - allow entry of granzymes - granzymes activate capases - apoptosis

Pathway 2: Expression of Fas ligand on CTLs
Fas ligand bind to Fas on target cell - induce apoptosis.

124
Q

What are the two types of memory T cells?

A

Effector memory T cells - retain adhesive properties - migrate to epithelia of skin and lungs - ready to respond

Central memonry T cells - circulate through blood and lymph node - ready for activation

125
Q

Define bystander activation of T cells

A

Memory T cells can be activated by high local levels of cytokines induced by unrelated pathogens

126
Q

How is immune response regulated?

A

Elimination of antigens -> remove the trigger

Apoptosis of antigen-specific lymphocyteswhen antigen, GFs and co-stimulatory factors are removed.

Inhibitory receptors like CD32 receptors or FcgamaII receptors - assess if sufficient amount of IgG - generate inhibitory signal

Regulatory B cells and T cells - release cytokines to control

127
Q

Events of immune response to primary extracellular bacterial infection

A

Check notes

127
Q

Events of immune response to primary viral infection

A

Check notes

PHAY00011 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions