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Maddy - Renal II > Immuno > Flashcards

Immuno Flashcards

1
Q

high renal oxygen demand is associated with

A

tubular O2 consumption used for solute reabsorption

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2
Q

sterile renal inflammation is induced by:

A

DAMPs

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3
Q

where do DAMPs come from in sterile inflammation

A
  • parenchymal kidney cells

- generated during ECM degradation and remodeling

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4
Q

role of native C reactive protein (CRP)

A

binds DAMPs and activates complement classical pathway

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5
Q

how do classically activated M1 macrophages induce inflammation in the kidney

A

microbial TLR-ligands, interferon gamma, PAMPs, DAMPs activate the macrophages which then perpetuate the acute phase of inflammation in the kidney

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6
Q

how do alternatively activated M2 macrophages participate in the immune response in kidneys

A

induced by IL-4, IL-13 –> important in tissue repair and renal fibrosis
- also anti-inflammatory

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7
Q

what two cytokines control renal fibrosis from M2 macrophages

A

IL-10

TGF-B

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8
Q

type II hypersensitivity

  • what antibodies
  • antigen form
  • mechanism
A
  • IgG and IgM
  • cell-bound
  • complement activation and cell lysis
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9
Q

examples of type II hypersensitivity

A

patient with anti-glomerular basement membrane antibody-mediated GN

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10
Q

type III hypersensitivity

  • what antibodies
  • antigen form
  • mechanism
A
  • IgG and IgM
  • solube
  • complexes deposited in tissues, complement recruits neutrophils, enzymes from neutrophils damage the tissue
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11
Q

examples of type III hypersensitivity

A
  • post-strep glomerulonephritis
  • rheumatoid arthritis
  • SLE
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12
Q

when are endothelial cells activated in immune response

A
  • ischemia induced glomeruonephritis
  • diabetes
  • sepsis
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13
Q

when are dendritic cells and macrophages activated in immune response

A

DC: acute injury and infectino
M: most diseases

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14
Q

what 2 cytokines control tissue repair and renal fibrosis

A

IL-10

TGF-B

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15
Q

why do M2 macrophages stimulate pericytes during repair

A

pericytes lead to the differentiation of myofibroblasts which then leads to production of ECM

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16
Q

role of Tregs in AKI

A

secrete TGF-B and IL-10

anti-inflammatory

17
Q

what are the targets for rejection in host versus graft transplants

A

histocompatibility antigens

18
Q

how can you increase the chances of survival in xenografts

A

inserting human genes into the genome of hte donor animal

19
Q

why is the father of a organ recipient a better fit for the transplant than the mother

A

the mother could have pregnancy-induced HLA sensitization, meaning they have pre-existing antibodies, which would lead to immediate hypersensitivity reactions

20
Q

what are the three most important pairs of class II HLA for transplantation

A

HLA-DR
HLA-DP
HLA-DQ

21
Q

when testing for class I HLA compatibility, what result would indicate identical HLA Ag

A

complement forms pores in the cells and dye accumulates in the cells

22
Q

when testing for class I HLA compatibility, what result would indicate non-identical HLA Ag

A

no dye accumulation because complement did not form pores in the cells

23
Q

host vs graft disease

A

recipient’s T cells attack the transplant

24
Q

graft vs host disease

A

T cells in transplant attack recipients tissues

25
Q

what happens if a second graft is performed from the same donor

A

the transplant is rejected more rapidly

26
Q

what cells cause acute rejection

A

Th1 cells and CTLs

27
Q

what cells cause chronic rejection

A

M2 macrophages and T cells

28
Q

what cells cause hyperacute rejection

A

preexisting antibodies and complement

29
Q

when and how does hyperacute rejection present

A

when: during surgery
how: thrombosis and occlusion of graft vessels

30
Q

when and how does acute rejection present

A

when: weeks to months
how: inflammation and leukocyte infiltration of graft vessels

31
Q

when and how does chronic rejection present

A

when: months to years
how: intimal thickening and fibrosis of graft vessels and graft atrophy

32
Q

2 reasons for hyperacute graft rejection

A
  1. ABO incompatibility
  2. recipient has been sensitized to donor MHC by previous transplants/blood transfusions/pregnancy –> Abs bind to endothelial cells –> complement –> endothelium death
33
Q

how does chronic graft rejection occur

A

indirect pathway

  • macrophages infiltrate and smooth muscle proliferation occurs
  • occlusion of blood vessels and ischemia of the organ occurs
34
Q

3 non-immunological factors in chronic rejection

A
  1. ischemia-reperfusion damage
  2. recurrence of the disease that caused failure of own kidney
  3. effects of nephrotoxic drugs like cyclosporine A
35
Q

does chronic rejection respond to immunosuppressive therapy

A

no

36
Q

who does graft versus host disease occur in and why

A

immunocompromised patients

- their immune system is unable to reject the allogenic cells in the graft

37
Q

where does acute GVHD occur and how does it appear clinically

A

where: epithelium in skin, liver, GI
how: rash, jaundice, diarrhea, GI hemorrhage

38
Q

where does chronic GVHD occur and how does it appear clinically

A

where: affected organ
how: fibrosis and atrophy of organ, dysfunction of organ, obliteration of small airways

Maddy - Renal II (6 decks)

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