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Medicine Unit 3 > IMMUNITY REVISION > Flashcards

IMMUNITY REVISION Flashcards

1
Q

what causes the cardinal signs of inflammation

A

caused by histamine release from mast cells, basophils and platelets, binds to histamine receptors and leads to vasodilation and exudation

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2
Q

what are the cardinal signs of inflamamtion

A

rubor
calor
dolor
tumour
functio laesa

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3
Q

what are the different barrier defences

A

flow of air or fluid
enzymes
low pH
defensins
normal microbia
tissue resident immune cells
cilitated cell
goblet cells
epithelial tight junctions

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4
Q

flow of air or fluid

A

reduces the change of mucroorganisms attaching

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5
Q

enzymes

A

secretions contain antimicrobial enzymes
lysozyme in tears

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6
Q

low ph

A

restricts which oathogens can survive if ingested

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7
Q

defensins

A

antimicrobial peptides disrupt the clel membranes and virus envelopes

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8
Q

normal microbia

A

outcompete potentiall harmful rganisms

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9
Q

tissue resident immune cells

A

recognsie
engulf
phagocytose and ill pathogens

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10
Q

cilitated cells

A

move mucus along to flush out thepathogens

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11
Q

goblet cells

A

produce mucus which acts as a sticky barrier

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12
Q

epithelial cells tight junctions

A

restrict movement of microorganisms deep into the tissue

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13
Q

migration of neutrophils in inflmmation

A
  • Margination: cells line up against the endothelium
  • Rolling: close contact with and roll along the endothelium
  • Adhesion: connecting to the endothelial wall
  • Emigration: cells move through the vessel wall to the affected area
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14
Q

what happens when no microbes are present

A
  • DAMPs/PAMPs bind to PRR’s
  • Activate cells
  • Induce inflammatory cytokine release
  • Trigger inflammation
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15
Q

what are the different types of PRR’s

A

toll like receptors
phagocytic receptors
NOD and RIG like receptors

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16
Q

toll like receptors

A

external or endosomal
change gene transcription and cytokine release

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17
Q

which toll like receptors are on the plasma membrane

A

TLR4
TLR5
TLR2
TLR1/6

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18
Q

which toll like receptors are endosomal

A

TLR3
TLR7
TLR8
TLR9

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19
Q

what binds to TLR 4

A

LPS

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20
Q

what binds to TLR 5

A

flagellin

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21
Q

what binds to TLR2, 1 and 6

A

lipoproteins

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22
Q

what binds to TLR 3

A

dsRNA

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23
Q

wat inds to TLR 7 and 8

A

ssRNA

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24
Q

what binds to TLR9

A

CpG DNA

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25
Q

phagocytic receptors

A

external
induce the uptake of pathogens into the endosomes and killing of the pathogen

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26
Q

what are the different phagocytic receptor

A

complement
savenger
mannose
Fc
C type lectin

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27
Q

NOD and RIG like receptors

A

cytoplasmic
change gene transcription
and cytokine release

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28
Q

extracellular TLR signalling

A
  • Binding of PAMP to PRR
  • Signal to nucleus
  • Adaptors containing TIR domains transmit message to cytoplasm
  • NFKB assembles and binds to DNA
  • Instructs cells to produce new proteins which initiate next stage
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29
Q

endosomal TLR signalling

A
  • Recognition of a pathogen within the endosome
  • Signal to the nucleus
  • Adaptors containing TIR domains transmit message to cytoplasm
  • Interferon response factors assemble and bind to DNA
  • Instructs cells to produce new proteins: interferons which direct immune responses against viruses and intracellular bacteria
  • IRF3: interferon B so antiviral response occurs
  • IRF7: type 1 interferons so antiviral response occurs
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30
Q

NOD and RIG signalling

A
  • Recognition of DAMP’s and PAMPs in the cytoplasm transmits signal to the nucleus
  • NLR aggregate and form inflammasome
  • Activates and causes release of pro-inflammatory cytokines
  • RLR aggregate and activate transcription factors leading to production of new proteins including type 1 interferons
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31
Q

macrophages and pathogens

A
  • Pathogen recognized by the PRR and macrophages activated
  • Phagocytosis induced
  • Pathogen is either internalized in a phagosome or activated macrophages make proinflammatory cytokines to attract other immune cells
  • Pathogen is killed by oxidative burst and digested enzymes
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32
Q

how do immune cells find pathogens

A

where the concentration of the chemokine is the highest

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33
Q

neutrophil arrival

A
  • Phagocytose similar to macrophages
  • Microbes are phagocytosed into phagosomes
  • Phagosomes fuse with the granules which contain antimicrobial enzymes, proteins and peptides
  • Microbes killed by digestion and respiratory burst
  • 3 types of granules: primary (azurophilic), secondary (specific) and tertiary (gelatinase)
  • Apoptosis and netosis: respiratory burst by producing toxic oxygen species to kill the bacteria
  • Netosis causes release of NETs: DNA covered in histone proteins and granule contents which trap the microbes
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34
Q

what happens if the pathogen isnt cleared

A
  • Release pro-inflammatory cytokines
  • Damaged blood vessels will produce bradykinins to increase vascular permeability and stimulate nerves causing pain
  • Then resolves in adaptive immunity
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35
Q

exampels of some acute phase proteins

A

Acute phase proteins: serum amyloid, C-reactive, fibrinogen, mannose binding lectin

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36
Q

complement pathway

A
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37
Q

howdo cells recognsie intracellular moleucles

A
  • Damage caused can be recognized by PRRs
  • PAMPs released from cells can also activate innate immune cells
  • Phagocyte will try and kill the bacteria by acidification and enzymatic digestion
  • Some thrive and survive
  • Others will penetrate cell from outside or escape from phagosomes into the cytoplasm
  • When in the cytoplasm the bacterial products can be recognsied by internal PRRs
  • Cytokines released to activate NK cells and adaptive immune cells
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38
Q

interferons

A

increase viral defences and reduce viral replication

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39
Q

tpye 1 interferons

A

Type 1: IFN alpha and beta, made by infected cells which increase anti-viral defence mechanisms in nearby cells
- IFNa and b bind to IFNa receptor
- Activation of genes which degrade viral RNA and stop protein synthesis needed to make viral capsues
- Recruit and activate NK cells
- NK cells kill by apoptosis: granules containing perforin and granzyme by recognizing altered self cells

40
Q

type 2 interferons

A

Type 2: IFN gamma released by adaptive immune cells

41
Q

type 3 interferons

A

Type 3: anti-viral and anti-fungal responses

42
Q

naive CD4 secreting IL-12 and IFN gamma

A

autoimmunity
intracellular pathogens
T helper 1 with T bet transcription factor
then T helper 1 will secrete IFN gamma and TNF

43
Q

naive CD4 secreting IL-2 and IL-4

A

extracellular pathogens, allergy and asthma
GATA 2 transcription factor to TH2
Th2 secretes IL4,5,13

44
Q

naive CD4 secreting TGF beta and IL-4

A

allergy, asthma, helminthes
TH9 by PU.1 and IRF4
secretes IL-9

45
Q

naive CD4 secreting IL-6 and 21

A

B cell help in the germinal centre
Bcl-6 will transcribe Tfh
which will secrete IL-21, 4 and IFN gamma

46
Q

naive CD4 secreting IL-1 and 23

A

extracellular bacteria, fungi and autoimmunity
RORyt will transcribe Th17
which will secrete IL-17 and IL-22

47
Q

naive CD4 secreting TGF beta and IL-2

A

immune tolerance, lymphocyte homeostasis
FOXp3 will transcribe Treg cells
which secrete TGF beta and IL-10

48
Q

naive CD4 secreting TNF and IL-6

A

autoimmunity
AHR will transcribe TH22
which secretes Il-22 and TNF alpha

49
Q

t celsl

A

cytotoxicity, help of other immune cells, regulation, originate in the bone marrow and mature in the thymus, express T cell receptors (heterodimeric) and will recognize peptides presented to it

50
Q

b cells

A

antibodies

51
Q

memory T and B cells

A

long-lived, trigger quicker and more effective immune response on second infection with the same pathogen

52
Q

professional APC’s

A

macrophages, B cells and dendritic cells

53
Q

dendriticc cells

A
  • Have MHC class 1 and 2 so can activate both CD8 and CD4
  • Migrate to secondary lymphoid tissue
  • Mature when stimulated by PAMP’s and DAMP’s
54
Q

cytotoxic T cells

A
  • MHC class 1, which presents antigens on all body cells, ecode for HLA A,B and C antigens
  • CD8 co receptor
  • kill virus infected cells directly
55
Q

T helper cells

A
  • MHC class 2, presents antigens only on professional antigen presenting cells, encode for HLA-DP, DQ and DR
  • CD4 co receptor
  • Produces cytokines to activate other immune cells and express surface molecules to affect other cell types
56
Q

MHC class 1 presentation

A
  • Infection of the body cell by the virus
  • Virus is chopped up by the proteosome
  • New viral particles are synthesized in the ER
  • Antigens loaded onto the MHC class 1 in the ER
  • Activates CD8 cytotoxic t cells
57
Q

MHC class 2 presentation

A
  • Phagocytosis of the pathogen by APC
  • Pathogen chopped up by phagolysosomes
  • Antigens loaded onto MHC class 2 in phagolysosome
  • Activates CD4 T helper cells
58
Q

3 signals for naive T cells to be activated

A
  1. Antigen binding to the T cell receptor: peptide- MHC to the TCR, an immune synapse will form if recognition occurs
  2. Co-stimulation: B7 molecules (CD80 and 86) on the APC binds to CD28 on the T cell
  3. Cytokines: APC produces cytokines that instruct the T cell to differentiate into the correct type of effector T cell
59
Q

what are the 2 cytotoxic T cell killing mechanisms

A

perforin/granzyme
Fas:FasL interaction

60
Q

perforin/ granzyme

A
  • Exocytosis of the lytic granules at the immune synapse
  • Perforins polymerise forming cylindrical pores in the target cells
  • Triggers the caspase cascade
61
Q

Fas:FasL interaciton

A
  • FasL is expressed by the cytotoxic T cells
  • Fas by the target cells
  • Activates FADD and then pro-caspase 8
  • Caspases are activated
  • Resulting in orderly destruction of the target cell
62
Q

how can a CD4 T cell activate a CD8 t cell

A
  • Activated CD4 T cell expresses CD40L and upregulates IL-2
  • This enhances APC survival and cross primes CD8 cytotoxic by enhancing APC activation
  • Increases B7 expression and CD70
  • Increases APC production of IL-12
63
Q

b cells activation

A
  • Antigen activates the B cell via the BCR, taken up, processed and presented on MHC class 2 to a specialized CD4 helper T cell
  • B cell will co-stimulate with CD4 helper T cell with CD40: CD40L respectively
  • CD4 helper T cell will instruct the B cell to produce a certain antibody type
  • B cell is activated, proliferates and differentiates into plasma cells and memory cells
  • IgM is the first antibody class to be made
64
Q

variable regions

A

detemrine antigen specificity

65
Q

constant region

A

determines antibody class
binds to Fc eceptors

66
Q

5 types of antibodeis

A

IgG
IgE
IgA
IgD
IgM

67
Q

IgG

A

high affinity and crosses the placenta

68
Q

IgE

A

parasite repsosnesand allergies

69
Q

IgD

A

basophils

70
Q

IgA

A

secreted at mucosal sites

71
Q

IgM

A

made on first encounter with an antigen

72
Q

5 functions of antibodies

A

neutralisation
opsonisation
complement activation
NK cell sensitisation
mast cell, eosinophil and basophil sensitisation

73
Q

neutralisation

A

bind bacterial toxins and virus particles, stop them binding receptors on the host cells, prevent tissue damage, IgA and IgG

74
Q

opsonization

A

antibodies that bind to pathogens, phagocytes recognize bound antibody via Fc receptor, trigger phagocytosis and killing, IgG

75
Q

complement activation

A

antibodies that bind pathogens and activate complement pathway, trigger formation of membrane attack complex and killing of pathogen, IgM and IgG

76
Q

NK cell sensitisation

A

antibodies against their viral proteins, may bind their target on surface of infected host cells, NK cells recognize bound antibody via Fc receptor and kill cells, IgG

77
Q

mast cell, eosinophil and basophil sensitisation

A

cross linking causes mast cell degranulation and releases mediators, eosinophils recognize IgE bound to parasites and release granules to kill parasite, basophils recognize IgD activating anti-microbial and pro-inflammatory mechanisms

78
Q

what is a primary lymphoid organ

A

site where T and B cells are made and matured

79
Q

exampels of primary lymphoid organs

A

bone marrow
thymus

80
Q

secondary lymphood organs

A

site where B and T cells can recognise antigen and beome activated to fight infeciton or cancer

81
Q

examples of secondary lymphoid organs

A

lymph nodes
spleen
MALT’s

82
Q

spleen in immunity

A
  1. Foreign antigen carried into the spleen from the splenic artery
  2. Into the marginal zone
  3. Captured by dendritic cells
  4. Dendritic cells and T cells move to the PALS from the splenic artery
  5. In the PALS dendritic cells activate helper T cells
  6. Activate B cells and activated B cells and helper T cells move to the primary follicles in the marginal zone
  7. Leads to production of secondary follicle in the germinal centre
83
Q

lymph nodes in immuntiy

A
  1. Antigen and APC from the tissue travel to the lymph node in the lymphatic fluid
  2. Antigens are processed by the resident dendritic cells in the paracortex
  3. Dendritic cells and B cells activate antigen specific helper T cells
  4. B cells also activated in the paracortex by antigen directly via the BCR and helper T cells
  5. Activated B and helper T cells form foci with proliferating B cells
  6. B cells and helper T cells migrate to primary follicles of the cortex and interact with the follicular dendritic cells
  7. Leads to production of a secondary follicle with a germinal centre and production of antibody producing plasma cell
84
Q

germinal centres

A
  • In the secondary lymphoid follicles
  • B cells proliferate and undergo somatic hypermutation to make better antibodies
  • Proliferating B cells seen in the centre, light and dark zones
  • Inactive B cells pushed towards the edge to form the mantle zone
  • B cells surrounded by a cuff of T helper cells
85
Q

wehat happens in the dark zone of a germinal centre

A

b cells mutate their genes

86
Q

what happens in the light zone of a germinal centre

A

b cells present to follicular t helper cells

87
Q

somatic hypermutation

A

immunoglobulin gene sequences are further mutated after rearrangement and binding to their antigen, V sequences are mutated resulting in more diversity and higher affinity

88
Q

affinity maturation

A

selection of B cells with the highest affinity BCR through interaction of follicular T helper cells

89
Q

what occurs after somatic hypermutation and affinity maturation

A
  • B cells move into the light zone
  • Receive a second signal from a T helper cell
  • Causes differentiation into either plasma cell or memory B cell
  • Can induce class switching of antibody
90
Q

class switching

A

make different types of isotypes with different constant regions

91
Q

2 types of MALT’s

A

BALTs: bronchus
GALTS: gut

92
Q

inductive sites

A

where B and T celsl are primed by antigen and differentiate into the effector cell

93
Q

effector site

A

where B and T cells migrate to carry out effector funcitons to clear pathogens

94
Q

microfold cells

A
  • Inductive sites
  • Broad processes in contact with the lumen
  • Deep invagination in basal membrane
  • Filled with clusters of B, T, dendritic cells and macrophages
  • Antigen is phagocytosed by the M cell
  • Transported and released into the basolateral pocket of the cell
  • Antigen taken up by the dendritic cells leading to activation or tolerization of T and B cells in the lamina propria
95
Q

what do plasma cells secrete

A

IgA and IgD

Medicine Unit 3 (28 decks)

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