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MII2 > Killing extracellular pathogens L22 > Flashcards

Killing extracellular pathogens L22 Flashcards

(46 cards)

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1
Q

2) DC activate T cells

A

when there is a pathogen in the body, DCs take the Ag to the LN where the naive T cells are
these Naive T cells interrogate DC to see if the Ag being presented is one they recognised

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2
Q

Th cells - helper

A

coordinates immune response
amplify innate immunity
expresses CD4 and recognises extracellular Ag presented by MHC 2

secretes IFN-Y to:
activates macrophages
inflammation
activation of T and B proliferation

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3
Q

Regulatory T cells - Treg

A

turn off immune response
express CD4 and recognise extracellular Ag presented by MHC 2

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4
Q

CTL - cytotoxic

A

kill infected cells
express CD8 and recognise intracellular Ag presented by MHC 1

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5
Q

3) T cells activate, divide and differentiate into effector cells

A

first antigen recognition from APC to naive T cell, causes activation and this secretes cytokines and cytokine receptor expression (IL-2 AND IL-2R)
proliferation occurs via mitosis and then differentiation - this occurs in lymphoid organs

differentiation of T cells is in the peripheral tissues, either becoming :
- effector T cell
- memory T cell

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6
Q

CD4+ receptor

A

activation of macrophages, B cells and other cells

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7
Q

CD8+ receptor

A

killing of targeted infected cells, macrophage activation

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8
Q

different Th cells

A

subsets are specialised at dealing with different infection types so it is important can differentiate into these to specialise their immune attack

Th1
Th2
Th17
Tfh

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9
Q

what does Th1 do

A

promotes cell-mediate immunity, targeting macrophages and causing activation of macrophage

secretes IFN-Y mostly, but also IL-2 and TNF-A

targets intracellular pathogens and cancer cells

IL-12 drives naive T cells to become Th1

can play a part in autoimmunity and chronic inflammation

migrate to infection site

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10
Q

what does Th2 do

A

this promotes humour (antibody mediated) immunity

producing cytokines IL-4, IL-5, IL-13

main role is activating eosinophils (IL-5), promoting B cells to switch to IgE (IL-4) , stimulation of mast cells and basophils, alternative macrophage activation

this attacks, kills helminths

can play a role in allergies

migrate to infection site

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11
Q

what does Th17 do?

A

enhances neutrophil-mediate response

produces IL-17, IL-21, IL-22 MAINLY

causes neutrophil recruitment (IL-17) and activation, can strengthen epithelial barrier (IL-22)

attacks extracellular bacteria and fungi, especially at mucosal barriers

can play a role in autoimmunity and inflammation

migrate to infection site

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12
Q

what does Tfh do

A

helps B cells in germinal centres - antibody production and isotype switching

produces IL-21 and IFN-Y or IL-4

promotes affinity maturation and class switching, essential for long -term humour immunity and supports generation of memory of B cell

these remain at LN to activate B cells

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13
Q

how does Th cell subset differentiation occur?

A

1st need signal 1 and 2 for T cell activation and clonal expansion via IL-2

then signal 3 directs T cell effector function - subset differentiation

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14
Q

signal 3 and effects for T cell differentiation

A

signal 3 is usually given by cytokines secreted from other cells (from APC) to tell T cell the infection type - bacteria, virus , parasite etc,
so it can differentiate into a specific type best for the type of microbe infection

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15
Q

IL-12

A

drives differentiation into Th1

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16
Q

IL-4

A

drives differentiation into Th2

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17
Q

TGF-Band IL-6/IL-23

A

drives differentiation into Th17

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18
Q

IL-6 and IL-21

A

drives differentiation into Tfh

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19
Q

TGF-B and IL-2

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A

drives differentiation into Treg

20
Q

activated and naive B cells

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A

activate B cells are known as plasma cells and secreted antibody is their effector molecule

naive cells do not produce Ab until activated, membrane bound antibody is the B cell antigen receptor

21
Q

naive B cells

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A

haven’t encountered antigens yet
express IgM and IgD on their surface
circulate in blood and lymph
awaiting activation by antigen and T cell help

22
Q

Plasma B cells - effector B cells - activated

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A

differentiated into antibody secreting cells
secrete large amounts of antibodies
short lived in circulation but long lived in bone marrow

23
Q

memory B cells

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A

formed after activation and class switching
long lived and quick responders to repeat infections
express class -switched BCRS

24
Q

IgM

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A

pentamer
first antibody made
strong complement activation
good at agglutination
fast responder
found on naive b cells

25
IgG
monomer most abundant in blood neutralisation opsonisation - phagocytosis aid crosses placenta protects foetus main antibody after vaccination
26
IgA
dimer with secretory component mucosal protection neutralisation of pathogens without inflammation passed to baby via breast milk mucosal barrier antibody
27
IgE
monomer binds to mast cells and basophils triggers histamine release defense against parasites key for allergies
28
IgD
monomer possible in role in b cell activation not much known co expressed with IgM on naive b cels
29
complement system 3 main functions
opsonisation to enhance phagocytosis stimulating inflammation by recruiting and activating immune cells lysising microbes and cells
30
complement mediated opsonisation
binding of C3b to microbe recognition of bound C3b by phagocyte C3b receptor CR1 phagocytosis and killing of microbe
31
complement mediated inflammation
C3a, C4a, C5a released during complement activation act locally similar to inflammatory cytokines to recruit cells to infection site and activate cells like neutrophils, lymphocytes and macrophages
32
complement mediated cytolysis
membrane attack complex MAC forms in membrane of bacteria to cause water to rush in, ions rush out and burst microbe can also kill host/foregin cells
33
steps of phagocytosis
1) phagocyte detects microbe via PRR, complement protein of Ab and then extends pseudopodia to engulf microbe 2) membrane invaginated forming an inside out vesicle called phagosome 3) phagosome fuses with lysosome to form a phagolysosome and this enzyme degrades microbe 4) chemical in phagolyosome active and digest microbe
34
vacuolar ATPases -phagosome killing mechanisms
these pump H+ ions into phagosome to acidify the environment lowers ph to activate enzymes and inhibit pathogen survival
35
ROS - respiratory burst - phagosome killing mechanisms
phagocyte oxidase converts O2 to superoxide to form H2O2 or OH radicals, this is toxic to bacteria and viruses
36
bleach bomb - phagosome killing mechanisms
MPO use H202 + CL- to form HOCL which is a potent microbicidal oxidant to kill bacteria by oxidising proteins lipids and DNA
37
proteolytic enzymes - phagosome killing mechanisms
neutrophils = elastase, cathepsins macrophages = lysosomal hydrolase these degrade bacterial proteins, cell walls and nucleic acids to destruct microbial components
38
nitric oxide and RNS - phagosome killing mechanisms
macrophages produce NO via iNOS to react with superoxide to form ONOO-, damages microbial DNA, proteins and membranes
39
nutrient deprivation - phagosome killing mechanisms
lactoferrin binds iron to limit avaliablty to pathogen scavenger proteins remove other essential nutrients starves microbes of key elements
40
antimicrobial peptides - defensives - phagosome killing mechanisms
insert into bacterial membranes to form pores to cause direct microbial lysis
41
antibodies make phagocytosis more efficient
Ab bind to microbe with high specificity and affinity phagocyte binds to Ab via Fc receptor (FcR) this is more efficient detection system than PRRS the binding of the Ab to FcR activates phagocyte for phagocytosis
42
neutrophil extracellular Traps NETS
neutrophil dies via NETosis nucleus swells and burst to extrude DNA like net the DNA has anti-microbial molecules attached like defenesins and proteases which trap and kill bacteria fungi, viruses = forming pus
43
neutralisation of microbes and molecules via Ab
1. antibodies prevent penetration of microbe through epithelial barrier 2. antibody blocks binding of microbe and infection of cells 3. antibody blocks binding of toxins to cellular receptors
44
granulocytes
these are pressure effect molecules in granules in cytoplasm that are ready to fire out when activated include mast cells, basophils, eosinophil, neutrophils
45
Antibody dependent cell mediated cytotoxicity
ADCC antibodies bind to target cell or microbe Fc portion of Ab binds to FcR on innate cell cel is activated if multiple FcR-Ab interactions occur cells firs out its granules at target destructive process and can cause lots of damage to healthy tissue
46
mast cell degranulation
weep response - cause liquid to flow from tissue into lumen to push things away from gut wall sweep response - release histamines to cause muscle contractions and push microbes out with faeces - this is what causes wheezing cytokines production - amplifies inflammatory response

MII2 (30 decks)

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