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Infection And Immunity > Immunity > Flashcards

Immunity Flashcards

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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
IgM
Agglutinates infectious agents
26
How antibodies attack parasites
Bind to surface antigen on the parasites Allow recruitment of eosinophils, cytotoxic T cells and neutrophils Degranulation attacks the parasite
27
How do bacteria and viruses evade antibody attack
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
28
Trypanosomes
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
29
3 stages of response to a new infection
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
30
Antigenic shift and drift | Influenza
Drift- alter epitopes in haemagglutinin, antibodies don't bind Shift- RNA segments exchanged, new haemagglutinin not recognised H2N2, H1N1
31
Structure of the influenza virus
``` Envelope covered in neuraminidase and haemagglutinin 8 ssRNA which encode 10 proteins PB1, PB2, PA, HA NA M1, M2, NS1, NS2 ```
32
The process of viral replication within cells | Response to acute infection
``` Attachment Penetration Uncoating Synthesis of viral mRNA -> protein + nucleic acid Assembly of capsids Release ``` Cytokines and the. Natural killer cells
33
Time scale of response to viral infection
1-2 interferon, TNF and IL2 3-4 natural killer cells 5+ T cell killing
34
The role of interferon
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
35
How are natural killer cells: Inhibited Activated
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
36
How does a cytotoxic T cell interact with infected cell
CD8 interacts by non specific adhesion to cell If there is antigen specific interaction, release of effector Death of cell
37
The immune synapse of T cells
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
How cytotoxic T cells kill
``` 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
T cell recognition restrictions
Recognises a specific complex of MHC and peptide
40
Definition of antibody avidity
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
Valency can affect antibody binding
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
Structures of the 5 antibody classes
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
Production of secretory IgA
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
Immunoglobulin for research
Papain- breaks heavy and light chains apart -> 2 fab fragments Pepsin- breaks chains so one fab fragment with 2 arms
45
How antibodies support host defence | 3
Neutralise toxins Neutralise pathogen for macrophage Activation of complement
46
Antibody levels in infants
Born with high IgG from mother IgM starts upon birth Own IgG not for 6 months Same for IgA
47
Locations of the 4 antibody classes
G- blood M- new response, heart A- open areas, respiratory and intestinal E- parasites and allergic. Cross linking -> histamine
48
Two colour immunefluorescence microscopy
Labeled antibodies reveal antigens in tissues Excited dye emits light Use to identify islets- beta by glutamic acid decarboxylase and alpha by glucagon
49
Affinity chromatography monoclonal antibody
Antibody attached to matrix Eluted by altering pH Can be revered to purify antibodies
50
Cell separation by magnetic beads
Antibody specific to cell surface attached to bead Iron mesh column made Cell bound by beads retained Removal of magnetic field elutes
51
Development of SCID
Lack of RAG 1 and 2 enzymes, no recombination possible. Treated by bone marrow transplant. Disabled virus to insert gene copy
52
Antibody diversity combinations | Human and mouse
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
Kappa light chain rearrangement
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
Recombination of mouse heavy chain
``` 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
Antibody class switching
``` 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
Increasing diversity by somatic hyper mutation
Antigen binds to activated B cell Induces point mutations in variable regions Enhance affinity -> affinity maturation of population
57
Assembly of the immunoglobulin
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
Sequence of B cell activation
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
Activation of B cell against virus
``` B cell binds to virus Ingests Presents peptides T cell activates B cell Produces lots of antibodies against coat ```
60
MHC genes
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
Mate selection and MHC
Relayed by androgen based pheromones | Women prefer odour of men with 0-1 similar alleles when not on the pill
62
MHC Class I pathway of antigen processing
``` 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
Cellular locations of TLRs
Located on cell surface detect pathogen | Within endosome membrane recognise internal PAMPS (ssRNA, dsRNA) after digestion
64
MHC Class II pathway (endosomic)
Antigen endocytosed Acidification of endosomes -> proteases active Peptide vesicle fuses with MHC vesicle Complex presented
65
How peptides bind to Class I
Anchor residues Strong residues in centre 9AAs long
66
How peptides bind to Class II
Anchor residues distributed 12-25 AAs Hang out end
67
Structure of the T cell receptor (TCR)
``` 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
What does ITAM stand for
Immunoreceptor tyrosine based activation motif
69
Roles of the CD4 and CD8 coreceptors
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
The B cell receptor complex
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
Cell adhesion molecules
Adhesion molecules on outside Antigen recognition inside TCR CD8 inside CD28 CD2 LFA-1 outside
72
Super antigens
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
Events in B cell activation
``` 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
Induction and function of cytokines
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
Tumour necrosis factor (TNF-a)
Cytokine produced by T helper cells Promotes leucocyte adhesion and extravasion Regulates macrophage activation T and B cell activation
76
Roles of TH1 and TH2 cells
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
4 main causes of autoimmunity
Release of sequestered antigens Molecular mimicry MHC class II expression of normal cells (high IFN-y) Activation of T cells by super antigens
78
Exposure to normally sequestered antigens
Trauma to eye Antigens releases travel to lymph nodes T cells activated Effector (memory) T cells encounter antigen in both eyes
79
Antigen mimicry
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
Type I hypersensitivity
IgE Antigen induces cross linking of IgE to mast cells and basophils Release of vasoactive mediators Hay fever, athsma
81
Type II hypersensitivity
IgG or IgM Antibodies against cell surface antigens Destruction through complement or ADCC Blood transfusion, haemolytic anaemia
82
Type III hypersensitivity
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
Type IV hypersensitivity
``` Cell mediated TH1 release cytokines -> macrophages and cytotoxic T cells Direct cell damage TH2 similar damage Dermatitis, graft rejection ```
84
Allergy
``` 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
The hygiene hypothesis
Allergy genes and clean environment -> allergy Mainly TH2 responses RSV infections increases athsma risk
86
Class switching interactions
B cell -> IgE CD40 signal -> class switch and CD80 expression More IL-4 production Food allergen patch testing
87
Erythroblastosis
Haemolytic disease of newborn Thesis negative motive, rhesus positive foetus B memory cells against first pregnancy -> antibodies Rhogam prevents B cell activation
88
Poison oak exposure
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
Transplantations
``` 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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