the adaptive immune response Flashcards

1
Q

the adaptive immune response (3)

A

specific to antigen, time lag and immunological memory

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2
Q

professional phagocytes are

A

monocytes, macrophages, neutrophils, tissue dendritic cells and mast cells

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3
Q

following ingestion of pathogen, what happens?

A

as well as ingesting, phagocytes especially macrophages can act as antigen presenting cells (APCs)

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4
Q

process of antigen presentation

A

phagocyte ingests a bacteria. Part of the bacteria (antigen) goes to the surface of the phagocyte, The phagocyte presents the antigens to T helper cells. this activates the helper t cell

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5
Q

Antigen presenting cells are

A

a link to the adaptive immune system

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6
Q

endoplasmic reticulum is associated

A

with degradation of microbe

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7
Q

transporters are associated

A

with antigen processing

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8
Q

cytolytic T I lymphocytes (CD8+) recognise

A

antigens presented by MHC I molecules

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9
Q

MHC I molecules

A

comprised of two polypeptides and present antigens originating from the cytosol

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10
Q

two major killing mechanisms of MHC I molecule

A

perforin and CD95 pathway

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11
Q

perforin killing mechanism of MHC I molecule

A

perforin delivered from cytoplasmic granules that fuse with the membrane of the APC forming pores to allow granzymes to enter the infected cell

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12
Q

CD95 pathway mechanism of MHC I molecule

A

FasL expression increases on CT and binds to Fas on the APC , leading to apoptosis

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13
Q

both perforin and CD95 pathways lead to

A

apoptosis rather than cell lysis, triggering the dead cells tone taken up by nearby macrophages

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14
Q

recognition of MHC II molecules by CD4+ T cells

A

recognise antigens presented on MHC II

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15
Q

MHC II molecule

A

two polypeptide- present antigens originating from the phagosome, peptides slightly longer than those presented by MHC I

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16
Q

difference in peptides presented by MHC II

A

MHC II present slightly longer peptides than those presented by MHC I

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17
Q

for recognition by CD4+ T ce;;s

A

costimulation needed- co-recepter in addition to MHC/ peptides/ TCR complex

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18
Q

costimulation

A

co-recepter in addition to MHC/ peptides/ TCR complex

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19
Q

CD8+ T cell and

A

MHC I

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20
Q

CD4+ T cell

A

MHC II

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21
Q

different Th produce diff

A

cytokines

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22
Q

Cytokines produced by Th1

A

IL-2, IFN- gamma, TNF- alpha, stimulating CTL cell

23
Q

Macrophage will release ……….. when CD4 co receptor forms with Th0 cell

24
Q

Th2 cell released

A

IL-4, IL-5, IL-6 –> stimulating B cells to differentiate and proliferate

25
B cells turn into
plasma cell
26
plasma cells produce
specific antiviral antibodies and bind to circulating virus/ | '
27
Th1 cell binds with
macrophage using CD28 and B7 receptors
28
Th0 binds to macrophage
using a T-ell receptor
29
CTL
cytotoxic T cell
30
Th1 cells and CTL cells
Th1 celleweive antigen from macrophage and this stimulates a CTL cell to form a CD8 coreceptor with a virally infected target cell, causing apoptosis of infected cells
31
B cells as ABCs
T- cells helped by CD4+ T cells
32
how does Th2 cell stimulate a plasma cell to produce specific antiviral antibodies
Th2 cell form a receptor complex with the B cell and stimulates it using IL-4, IL-5 and IL-6 and these cause the B cell to proliferate and differentiate
33
once exposed to TB two possibilities
either the immune system is adequate and there will be no infection or if dysfunctional infection will occur and then depending on the adequacy of the adaptive immune system the disease will either be active or alent
34
if latent, if the adaptive immune system fails
reactivation will occur
35
often Mtb will remain
latent forever - contained in granuloma
36
role of B cells in turberculosis
normally antibody producing cells- also a source of cytokines for further lymphocyte and macrophage recruitment
37
which cells are a source of cytokines for further lymphocyte and macrophage recruitment
B cells
38
stages of granulation which make the infection latent
infection, innate granuloma, imune granuloma, chronic fanuloma
39
what is a chronic granuloma made up of
monocytes, neutrophils, macrophages, dendritic cells, t cell, coma macrophages, epithelia macrophage and coated n a fibrotic encapsulation
40
the efficacy of antibody mediated immunity against microbes is established by three general approaches
1) presence of antibodies benefits the host 2) as the conc of antibodies increases, susceptibility to dies and infection decreases 3) if immune system is not producing an adequate number of antibodies, then increased likelihood of disease
41
have any of the antibody criteria been met for TB
NO- however relatively simple view that M.tb is an intracellular pathogen and thus outside the reach of antibodies- dismisses the number of mechanisms by which antibody mediated immunity can modify the outcome of bacterial intracellular pathogenesis through effects from opsonisation to activation of FcR
42
what role for PRRs in M.tb
in order to detect pathogens such as bacteria and viruses the immune system is equipped with receptors called pattern recognition receptors that are specialised in their recognition. mainly expressed by antigen presenting cells such as dendritic cells and macrophages but are also found in other immune and non-immune cells
43
PRRs
pattern recognition receptors- specialised in their recognition and key elements of the innate immune system
44
PRRs are mainly expressed on
dendritic and macrophage cells
45
PRR are divided into four families
Toll like receptors, Nucleotide oligomerisation receptors, C-type lectin receptors,, RIG 1 like receptor
46
PRRS are found in three strategic places
the cell surface to recognise extracellular pathogens such as bacteria or fungi; in the endosomes where they sense intracellular invaders such as virus and finally in the cytolasm
47
CLR and TLR are found
in the cell surface membrane
48
NLR and RLR are found
in the cytoplasm
49
TLR are found
in the membrane and in endosomes
50
which proinflmmatory cytokine is linked to mycobacteria (M.tb)
TNFalpha is a prototype pro inflammatory cytokine which is produced by phagocytic cells activated with mycobacteria
51
mice deficient in TNFalpha produvyion or receptor
exhibit increase susceptibility to Mtb infection
52
upon phagocytosis, phagocytic cells produce
IL-1- these recruit NK cells at the infection site. Where IL-12 and IL- 18 promote IFNgamma production which then exerts protective immune responses
53
IL-12 and IL-18
promote IFNgamma production which then exerts protective immune responses