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Infection And Immunity > Immunity > Flashcards

Immunity Flashcards

1
Q

The 4 definitions of inflammation

A 
Calor- heat
Dolor- pain
Rubor- redness
Tumor- swelling
Due to effects of local cytokines made by WBCs
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2
Q

The inflammatory response

A

Chemotaxis of phagocytes
Psuedopodia extends around agent
Lysosomes + phagosome -> phagolysosome
Antigenic peptides displayed in an MHC class II
Macrophages then release cytokines causing vasodilation
Then release inflammatory mediators which cause the pain

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3
Q

The 3 types of antigen presenting cell

A

Dendritic- can activate T cells in lymphatic organs
Macrophage- present peptide on MHC II for T helper
B lymphocytes- present on MHC class II

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4
Q

The activation of macrophages

A

Bacteria bind to PAMPS
Signalling through TLRs -> cytokine and chemokine production
Bacteria then ingested
Antibodies bind to bacteria, and complement deposits C3b. Antibody binds to Fc receptors and the C3b binds to CR1 receptors

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5
Q

Bacterial escape strategies from phagocytosis

A 
Toxin release
Protein A- prevent opsonisation
Capsule prevents contact
Inhibit fusion
Escapes into the phagocyte
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6
Q

3 basic actions of complement

A

Bacterial lysis
Chemotaxis of phagocytes
Opsonisation of bacteria

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7
Q

The classical pathway of complement

A

Antigen antibody complex is formed
C1q interacts with antibodies or surface
C3 convertase -> C3a and C3b

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8
Q

The mannose binding lectin pathway of complement

A

Mannose binding lectin or fiction binds to carbohydrate

C3 convertase -> C3a and C3b

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9
Q

The alternative pathway of complement

A 
C3 -> C3(H2O)
C3 convertase deposited 
C3(H2O) + factor D and factor B and factor P
Forms C3BbB on the surface
Convertase -> C3b bound
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10
Q

Results of the combined complement pathways

A

C3b bound, C3a released
C3a and C5a recruit phagocytes
Phagocytes bind to C3b with CR1 receptors

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11
Q

Actions of anaphylatoxins

A

C3a and C5a
Degranulation of mast cells -> histamine
Local oedema, leading to more anaphylatoxins

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12
Q

Action of chemotaxins

A

C5a

Attracts phagocytes and neutrophils

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13
Q

Assembly of the membrane attack complex

A 
C5b + C6 + C7
C5b67 binds to the membrane via C7
C8 binds and inserts into membrane
C9 binds and polymerises (C5b678) 
Lots of C9 molecules bind to form a pore which lyses the cell
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14
Q

Opsonisation

A

Phagocytosis enhanced if C3b bound. C5a also contributes.

C5a -> activates CR1 receptor -> CR1 binds to C3b

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15
Q

Regulation of complement

A

CD59 (protectin) binds to the C5b678 complex.

Prevents the insertion of C9s

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16
Q

Gram negative evasion of complement

A

Polysaccharides - prevent MAC insertion
Outer membrane protein- MAC interacts, does not insert
Elastase- C3b and C5a not activated

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17
Q

Gram positive evasion of complement

A

Peptidoglycan- MAC can’t insert

Capsule- C3b not deposited

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18
Q

Viral evasion of complement

A

Mimic complement regulatory proteins

E.g. Herpes simplex, Epstein barr

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19
Q

Development of B lymphocytes

A

B cell precursor rearranges genes in bone marrow
Any bound to cell surface removed
Mature B cell activated -> lymphoid organs
Divide into plasma and memory cells

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20
Q

Development of T lymphocytes

A

Arranges receptor genes in the thymus
Those interacting with self antigen removed
Encounter antigen in the lymphoid organs
Activated, proliferate and eliminate

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21
Q

Where are MHC I and MHC II found

A

MHC I - cells of body with a nucleus

MHC II - immune cells that can present to T cells

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22
Q

Secretory IgA dimers

A

Blocks binding of virus/bacteria to host cells

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23
Q

IgG, IgM and IgA

A

Blocks fusion of viral envelope with host cell membrane

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24
Q

IgG and IgM

A

Improves phagocytosis

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25
Q

IgM

A

Agglutinates infectious agents

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26
Q

How antibodies attack parasites

A

Bind to surface antigen on the parasites
Allow recruitment of eosinophils, cytotoxic T cells and neutrophils
Degranulation attacks the parasite

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27
Q

How do bacteria and viruses evade antibody attack

A

Have Fc receptors on surface which causes the antibody to bind upside down. These then fill the space stopping more antibodies from binding.
S.pneumoniae is sub type specific, need to wait until specific antibody developed for immune response

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28
Q

Trypanosomes

A

Changes VSG coat, new antibody needed each time
Antigenic shift- duplication of gene segments and translocation to expression site near telomere
VSG coat gained when progresses to salivary glands of tetse fly

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29
Q

3 stages of response to a new infection

A

Innate- non specific effectors
Early induced innate- inflammation recruitment
These both rely on TLR receptors
Adaptive immune response- antigen to lymphoid organs, recognition by B and T cells. Clonal expansion and differentiation

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30
Q

Antigenic shift and drift

Influenza

A

Drift- alter epitopes in haemagglutinin, antibodies don’t bind
Shift- RNA segments exchanged, new haemagglutinin not recognised
H2N2, H1N1

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31
Q

Structure of the influenza virus

A 
Envelope covered in neuraminidase and haemagglutinin 
8 ssRNA which encode 10 proteins
PB1, PB2, PA, HA
NA
M1, M2, NS1, NS2
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32
Q

The process of viral replication within cells

Response to acute infection

A 
Attachment
Penetration
Uncoating
Synthesis of viral mRNA -> protein + nucleic acid
Assembly of capsids
Release

Cytokines and the. Natural killer cells

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33
Q

Time scale of response to viral infection

A

1-2 interferon, TNF and IL2
3-4 natural killer cells
5+ T cell killing

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34
Q

The role of interferon

A

Cytokines produced
IFNa IFNb in response to dsRNA, recognised by TLR3. Resistance state.
Induce enzymes that inhibit viral replication and translation
IFNy secreted by T cells and NK cells, boosts antigen processing and presentation

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35
Q

How are natural killer cells:
Inhibited
Activated

A

Inhibited by MHC on normal cells
Interferon increases MHC I expression and so protects

Without MHC, recognises carbohydrate on the cell
Triggered by activating receptors
Releases granule contents inducing apoptosis

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36
Q

How does a cytotoxic T cell interact with infected cell

A

CD8 interacts by non specific adhesion to cell
If there is antigen specific interaction, release of effector
Death of cell

37
Q

The immune synapse of T cells

A

Supramolecular activation complex (SMAC):
pSMAC peripheral, cSMAC Central
Adhesion proteins hold cells together while TCR and MHC communicate
Reorganisation of cytoskeleton and release of effector molecules

38
Q

How cytotoxic T cells kill

A 
Calcium dependent release of granules 
Perforin- directs entry of granule contents to cytosol
Granzymes- serine proteases
granulysin- anti microbial
-> apoptosis
Then ingested by phagocytic cells
39
Q

T cell recognition restrictions

A

Recognises a specific complex of MHC and peptide

40
Q

Definition of antibody avidity

A

The overall strength of binding to an antigen
Both V regions can bind
Combined strength of both binding sites, more avidity
IgM is a pen tamer, high avidity

41
Q

Valency can affect antibody binding

A

Antibodies bind to surface
Valency = number of antibodies that can bind at a time
Space issues limit the number of antibodies
Viruses that have Fc receptors bind antibody upside down so largely decrease valency

42
Q

Structures of the 5 antibody classes

A

IgG - 2H 2L
Light chain is kappa or lambda
IgM - pentamer with J chain in centre
IgA is a dimer joined by J chain

43
Q

Production of secretory IgA

A

Muscoal epithelial cells in digestive, respiratory and genital, saliva, lacrimal
Dimer if IgG binds to a poly Ig receptor on basolateral membrane and is endocytosed
Receptor is cleaved, leaves with component wrapped around (J chain)

44
Q

Immunoglobulin for research

A

Papain- breaks heavy and light chains apart -> 2 fab fragments
Pepsin- breaks chains so one fab fragment with 2 arms

45
Q

How antibodies support host defence

3

A

Neutralise toxins
Neutralise pathogen for macrophage
Activation of complement

46
Q

Antibody levels in infants

A

Born with high IgG from mother
IgM starts upon birth
Own IgG not for 6 months
Same for IgA

47
Q

Locations of the 4 antibody classes

A

G- blood
M- new response, heart
A- open areas, respiratory and intestinal
E- parasites and allergic. Cross linking -> histamine

48
Q

Two colour immunefluorescence microscopy

A

Labeled antibodies reveal antigens in tissues
Excited dye emits light
Use to identify islets- beta by glutamic acid decarboxylase and alpha by glucagon

49
Q

Affinity chromatography monoclonal antibody

A

Antibody attached to matrix
Eluted by altering pH
Can be revered to purify antibodies

50
Q

Cell separation by magnetic beads

A

Antibody specific to cell surface attached to bead
Iron mesh column made
Cell bound by beads retained
Removal of magnetic field elutes

51
Q

Development of SCID

A

Lack of RAG 1 and 2 enzymes, no recombination possible. Treated by bone marrow transplant.
Disabled virus to insert gene copy

52
Q

Antibody diversity combinations

Human and mouse

A

Human- 48VH 23DH 6JH 8CH. 41vk 5jk
Mouse- 134VH 13DH 4JH 8VH. 85vk 4jk 1ck
85 x 4= 340 light chain, 6968 heavy. 2.4 mil

53
Q

Kappa light chain rearrangement

A

After heavy chain
One of 2 light chains rearrange
VK or VL genes
VK or VL + J + Ck or CL (depending on V)-> RNA

54
Q

Recombination of mouse heavy chain

A 
D segment recombines with J 
V + DJ -> VDJ
C + VDJ -> CVDJ always Cu in Virgin B cell
Can be Cs in non Virgin
CVDJ -> heavy chain
Done by enzymes RAG-1 and RAG-2

IgM has Cu and IgD produced later with Cs

55
Q

Antibody class switching

A 
Stimulated by T cells and IL-4
Move VDJ to another constant region
Recognised by enzymes because of repetitive DNA switch site
Cannot revert after loop excised
Only class changed not specificity
56
Q

Increasing diversity by somatic hyper mutation

A

Antigen binds to activated B cell
Induces point mutations in variable regions
Enhance affinity
-> affinity maturation of population

57
Q

Assembly of the immunoglobulin

A

Chains synthesised on seperate ribosomes
Disulphide bonds and glycosylation in rough ER
Taken to Golgi and packaged
Membrane IgG has extra transmembrane segment to anchor

58
Q

Sequence of B cell activation

A

TH expresses CD40L
Cd40 and cd40L -> signal
B7-CD28 co stimulation
B cell expresses cytokine receptors
Binds cytokines from T cell -> differentiation
More IgG secondary response
T cells activate B cells which recognise same pathogen but not epitope

59
Q

Activation of B cell against virus

A 
B cell binds to virus
Ingests
Presents peptides
T cell activates B cell
Produces lots of antibodies against coat
60
Q

MHC genes

A

Most polymorphic genes
Chromosome 6
HLA a,b,c,d. D divided to DP DQ DR
Allele expression linked to diabetes and autoimmunity
Individuals heterozygous for each locus, no silencing

61
Q

Mate selection and MHC

A

Relayed by androgen based pheromones

Women prefer odour of men with 0-1 similar alleles when not on the pill

62
Q

MHC Class I pathway of antigen processing

A 
Viral protein created with ubiquitin (conformational change unblocking PA28)
Immunoproteasome -> proteolysis
TAP 1 and TAP 2 transport to ER
B2-micro globulin binds to calnexin
Peptide binds to heavy chain via tapasin
This forms receptor -> cell surface
HCMV can produce immunoevasins
63
Q

Cellular locations of TLRs

A

Located on cell surface detect pathogen

Within endosome membrane recognise internal PAMPS (ssRNA, dsRNA) after digestion

64
Q

MHC Class II pathway (endosomic)

A

Antigen endocytosed
Acidification of endosomes -> proteases active
Peptide vesicle fuses with MHC vesicle
Complex presented

65
Q

How peptides bind to Class I

A

Anchor residues
Strong residues in centre
9AAs long

66
Q

How peptides bind to Class II

A

Anchor residues distributed
12-25 AAs
Hang out end

67
Q

Structure of the T cell receptor (TCR)

A 
Resembles fab fragment
Va and Vb at top, Ca and Cb at bottom
Cytoplasmic tail in membrane
Full complex = TCR and 6 CD3
CD3 needed for TCR chain expression
Have ITAM tails that signal cell
These ITAMS recruit transcription factors -> cytokines
Cancer causes zeta down regulation
68
Q

What does ITAM stand for

A

Immunoreceptor tyrosine based activation motif

69
Q

Roles of the CD4 and CD8 coreceptors

A

D1 of CD4 binds to MHC II on APC cell
Both CD8 chains bind to MHC I on virally infected cell
Help stabilise T cell MHC binding

70
Q

The B cell receptor complex

A

Membrane bound IgM and Iga and Igb
IgM recognises and binds antigen but cannot send its own signal
The Iga and Igb then signal interior through ITAM

71
Q

Cell adhesion molecules

A

Adhesion molecules on outside
Antigen recognition inside
TCR CD8 inside
CD28 CD2 LFA-1 outside

72
Q

Super antigens

A

Can override T cell specificity
Activate up to 25% of T cells by binding to all TCRs with VB sequence
Bind to T cell and MHC on outer edge
-> cytokine Storm
Bacterial- soluble exotoxins
Viral- membrane embedded
Staphylococcus- enterotoxin -> SEC3 and SEB

73
Q

Events in B cell activation

A 
TH expresses CD40L
Interaction of CD40 (b cell) + CD40L -> signal 2
B7-CD28 provides co stimulation
B cell expresses receptors for cytokines
Binds cytokines released form t helper
B cell differentiation
74
Q

Induction and function of cytokines

A

Cytokine binds to receptor -> dimerisation of receptor polypeptides
Activation of signalling, switching on genes
IL-2 - a and b subunits bind to cytokine, y signals cell.
Monoclonal antibodies against IL-2 chain used for transplants

75
Q

Tumour necrosis factor (TNF-a)

A

Cytokine produced by T helper cells
Promotes leucocyte adhesion and extravasion
Regulates macrophage activation
T and B cell activation

76
Q

Roles of TH1 and TH2 cells

A

TH1- activate infected macrophages via IFN-y
TH-2 - produces IL-4/5 stimulates B cell to produce antibodies, mast cells, eosinophils
They both inhibit each other

77
Q

4 main causes of autoimmunity

A

Release of sequestered antigens
Molecular mimicry
MHC class II expression of normal cells (high IFN-y)
Activation of T cells by super antigens

78
Q

Exposure to normally sequestered antigens

A

Trauma to eye
Antigens releases travel to lymph nodes
T cells activated
Effector (memory) T cells encounter antigen in both eyes

79
Q

Antigen mimicry

A

Primed T cell only require 1 signal
Streptococcus attacks heart valve -> rheumatic fever
In diabetes, effector T cell recognises peptides and kills B cell
No insulin made
Myasthenia- ACH receptors attacked

80
Q

Type I hypersensitivity

A

IgE
Antigen induces cross linking of IgE to mast cells and basophils
Release of vasoactive mediators
Hay fever, athsma

81
Q

Type II hypersensitivity

A

IgG or IgM
Antibodies against cell surface antigens
Destruction through complement or ADCC
Blood transfusion, haemolytic anaemia

82
Q

Type III hypersensitivity

A

Immune complex
AG-ab complex activate complement and infiltration of neutrophils
Immune complexes not broken down by complement or macrophage
Accumulation of complexes
Serum sickness, arthritis, lupus, glomerulonephritis

83
Q

Type IV hypersensitivity

A 
Cell mediated
TH1 release cytokines -> macrophages and cytotoxic T cells
Direct cell damage
TH2 similar damage
Dermatitis, graft rejection
84
Q

Allergy

A 
Type I hypersensitivity
IgE cross linked on mast cell
Pollen can bind 2 adjacent IgE
Mast cells secrete granules
Derp1- from dust mites -> epithelial damage
Ragweed- sneezing, eyes,
85
Q

The hygiene hypothesis

A

Allergy genes and clean environment -> allergy
Mainly TH2 responses
RSV infections increases athsma risk

86
Q

Class switching interactions

A

B cell -> IgE
CD40 signal -> class switch and CD80 expression
More IL-4 production
Food allergen patch testing

87
Q

Erythroblastosis

A

Haemolytic disease of newborn
Thesis negative motive, rhesus positive foetus
B memory cells against first pregnancy -> antibodies
Rhogam prevents B cell activation

88
Q

Poison oak exposure

A

Type IV
Pentadecacatechol complexed to skin proteins
Langerhans take up and present MHC II
IFN-y, MCP-1, MIF released from TH1 binding to MHC
cytokines cause blistering

89
Q

Transplantations

A 
Autograft- same person
Allograft- immunosuppression needed (not corneal)
Xenografts- different species
B -> AB
But not AB -> B

Infection And Immunity (2 decks)

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