T1D summary Flashcards

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1
Q

mediators of B cell death

A

CD8
CD4- Th1 and Th2
Macrophages
B cells

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2
Q

if B cells are infected with an enterovirus they will express

A

VP1

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3
Q

VP1 expression is also correlated with increased..

A

PKR and Mda5

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4
Q

PKR mediates

A

translational arrest

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5
Q

Mda5

A

unregulated IFN-1- stimulates other cells around to stop protein synthesis- apoptosis

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6
Q

both PKR and Mda5 stop labile proteins being produced e.g.

A

Mlc-2

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7
Q

Mlc-2

A

usually prevents apoptosis

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8
Q

concept of insulitiis

A
  • autoantibodies
  • B cell and antibody response
  • destruction of cells which overexposes HLA-1 (binding region on MHC-1)
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9
Q

HLA-1

A

binding region on MHC I

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10
Q

autoantibodies in T1 diabetes do not themselves

A

cause β-cell destruction, but rather reflect autoimmune activity; the β-cell destruction is mediated through T-cell

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11
Q

enterovirus implicated

A

cocksackie virus B

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12
Q

how do virus’ infect B cells

A

hijack CAR receptors and enter the B cell (alpha cells have better immune response), because of insulin granules

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13
Q

CAR found on

A

insulin granules

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14
Q

virus convert RNA into

A

sdRNA

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15
Q

persistent infection

A

virus evades immune system- staying the B cell surviving

- doesn’t cause cell to die or evoke an immune response

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16
Q

how does persistent infection occur

A

viral replication complex

17
Q

the viral replication complex

A

stops recognition of virus and avoids cellular response by stopping production of sdRNA

18
Q

viral replication complex means that virus’ can

A

permits within B cell without triggering acute immune response

19
Q

persistent infection is a reason for

A

late onset- something trigger virus to start replicating dsRNA, meaning it is recognised by the immune system

20
Q

acute infection

A

virus starts producing dsRNA rapidly (no viral replication complex), meaning immune system destroys straight away

21
Q

acute infections are characterised by

A

sudden onset

22
Q

biology of +ve single stranded viruses

A

ssRNA uses reverse transcriptase to convert ssRNA to dsRNA

23
Q

dsRNA

A

evokes a strong immune response- not human (unless within viral replication complex)

24
Q

ssRNA has a specific surface protein which

A

binds to CAR receptor - increasing uptake

25
Q

vaccine development

A

difficult to identify an immunogenic antigen produced by the virus
- may evoke an autoimmune repsonse

26
Q

why is diabetes not an infectious disease

A
  • won’t get the disease unless have the genetics for it
27
Q

genetics variation which increases susceptibility to T1D

A

if you have polygenic mutations (PKR and Mda5)- may have increased susceptibility to B cell destruction by virus’

28
Q

most diabetes is

A

polygeneic

29
Q

name two non polygenic T2D

A
  • neonatal (ABCC8, KCNJ11)

- mody (HNF1a, HNF1b, HNF4b and glucokinase)

30
Q

GAD

A

glutamic acid decarboxylase- antigen found on surface or B-cells

31
Q

anti-GAD antibodies found in how many patients

A

50-70%- usually later stage