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Immunology > Immunosupression > Flashcards

Immunosupression Flashcards

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
Q

which bacterial cytotoxic drugs reduce the expression of cytokines such as IL-2 which is a growth signal for t cells

A

cyclosporin A and tacrolimus

26
Q

what are the negatives of bacterial cytotoxic drugs

A

indescriminant, toxic to kidneys and expensive

27
Q

how does rapamycin cause t cells to die

A

it blocks the late stages of activation

28
Q

why is antibody therapy preferable to immunosupressive cytotoxic drugs

A

they interfere in a non toxic, more specific manner

29
Q

how do depleting antibodies work

A

trigger destruction of lymphocytes by macrophages and NK cells

30
Q

how do non depleting antibodies work

A

they block the function of a target protein without killing the cell

31
Q

how can antibodies be used in organ transplant

A

perfusion of the organ before transplantation with Abs that react with APCs targetting them for destruction

32
Q

how can Ab therapy be used to treat autoimmune disease

A

to modify and reduce the immune response

33
Q

which antibodies can be used in treatment of RA

A

anti-TNFa antibodies eg infliximab, etanercept

anti-IL-1 eg Anakinra

34
Q

what is the role of IFNg in TH1 response

A

activate macrophages and drive inflammatory response

35
Q

which sort of Thelper response is autoinflamatory disease related to

A

th1

36
Q

how does skewing the response from IgE to IgG and IgA in allergy reduce allergic symptoms

A

these Igs bind the allergen rather than binding mast cells and causing degranulation

37
Q

how can TH2 cells be primed to produce IL-4 and TGF-b without activating TH1 or antibody response

A

with peptide allergens

38
Q

how does EBV cause immunosuppresion

A

encodes a homologue of IL-10 which inhibits TH1 lymphocytes, reducing IFNg production

39
Q

which cells does HIV infect

A

CD4+ Tcells, DCs and macrophages

40
Q

how does HIV kill the cells it infects

A

direct viral killing, increased susceptibility to apoptosis, killing by CD8+ cells which recognise infected CD4+ cells

41
Q

how does mycobacterium leprae cause immunosuppression

A

suppresses cell mediated immunity (lepromatus leprosy) or cell mediated antibacterial response

Immunology (11 decks)

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