Immunosupression Flashcards

(41 cards)

1
Q

how does treating allergy with antigen in desensitisation regimes work

A

it diverts the response from TH2 to TH1 to produce IgG instead of IgE

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2
Q

what method other than desensitisation is used to treat allergy

A

specific inhibitors to block effects of inflamatory mediators produced by mast cells

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3
Q

why is autoimmune disease hard to control

A

because response not recognised until its well established

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4
Q

how is autoinflamatory disease treated

A

cortico steroids, cytotxic drugs

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5
Q

why does treatement of autoinflammatory disease often lead to opportunistic infection

A

because treatment is non specific so entire immune system is compromised

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6
Q

which molecules are primarily responsible for graft rejection

A

MHC molecules

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7
Q

what are the two ways in which alloantigens are recognised

A

the donor APCs migrate to lymphnodes or allogenic proteins are taken up by host APCs and presented to Tcells

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8
Q

how rapidly does hyperacute rejection occur

A

24hrs

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9
Q

what is the cause of hyperacute rejection

A

preexisting antibodies from a previous transplant or blood transfusion against MHC and blood type specific antigens

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10
Q

what is the result of hyperacute rejection

A

complement and blood clotting cascades block the blood vessels of the graft

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11
Q

what occurs in graft versus host rejection

A

mature t cells in the donor tissue recognise host tissues causing inflammatory response

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12
Q

what sort of immunosupressive drugs are synthetic analogues of cortisol

A

corticosteroids

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13
Q

how do corticosteroids work

A

they bind intracellular receptors and are then transported into the nucleus where they control transcription

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14
Q

what are the effects of corticosteroids

A

anti inflammatory

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15
Q

which inflammatory cytokines are reduced by corticosteroids

A

IL-1 TNFa IL-3 IL-4 and IL-5

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16
Q

how does decreasing the expression of adhesion molecules reduce inflammation by corticosteroids

A

wbcs are less likely to migrate from blood vessels

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17
Q

how does increasing the expression of endonucleases as a result of corticosteroids have an inflamatory effect

A

increases apoptosis in lymphocytes and eosinophils

18
Q

how do the immunosuppresive drugs azithrioprene and mycophenolate work

A

interfere with dna synthesis

19
Q

how does the immunosuppresive drug cyclophosphamide work

A

it alkylates dna

20
Q

Which type of fungus is cyclosporin A derived from

A

Tolypocladium inflatum

21
Q

which bacteria is tacrolimus derived from

A

Streptomyces tsukubaensis

22
Q

which bacteria is rapamycin derived from

A

Streptomyces hygroscopicus

23
Q

how do cyclosporin A, tacrolimus and rapamycin work

A

they bind immunoflins and interfere with clonal expansion of lymphocytes

24
Q

how does cylcosporin A block t cell proliferation

A

inhibits the Ca2+ activated enzyme calcineurin

25
which bacterial cytotoxic drugs reduce the expression of cytokines such as IL-2 which is a growth signal for t cells
cyclosporin A and tacrolimus
26
what are the negatives of bacterial cytotoxic drugs
indescriminant, toxic to kidneys and expensive
27
how does rapamycin cause t cells to die
it blocks the late stages of activation
28
why is antibody therapy preferable to immunosupressive cytotoxic drugs
they interfere in a non toxic, more specific manner
29
how do depleting antibodies work
trigger destruction of lymphocytes by macrophages and NK cells
30
how do non depleting antibodies work
they block the function of a target protein without killing the cell
31
how can antibodies be used in organ transplant
perfusion of the organ before transplantation with Abs that react with APCs targetting them for destruction
32
how can Ab therapy be used to treat autoimmune disease
to modify and reduce the immune response
33
which antibodies can be used in treatment of RA
anti-TNFa antibodies eg infliximab, etanercept | anti-IL-1 eg Anakinra
34
what is the role of IFNg in TH1 response
activate macrophages and drive inflammatory response
35
which sort of Thelper response is autoinflamatory disease related to
th1
36
how does skewing the response from IgE to IgG and IgA in allergy reduce allergic symptoms
these Igs bind the allergen rather than binding mast cells and causing degranulation
37
how can TH2 cells be primed to produce IL-4 and TGF-b without activating TH1 or antibody response
with peptide allergens
38
how does EBV cause immunosuppresion
encodes a homologue of IL-10 which inhibits TH1 lymphocytes, reducing IFNg production
39
which cells does HIV infect
CD4+ Tcells, DCs and macrophages
40
how does HIV kill the cells it infects
direct viral killing, increased susceptibility to apoptosis, killing by CD8+ cells which recognise infected CD4+ cells
41
how does mycobacterium leprae cause immunosuppression
suppresses cell mediated immunity (lepromatus leprosy) or cell mediated antibacterial response