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CPR Exam 2 > Immunological Aspects Of The Renal System - Shnyra > Flashcards

Immunological Aspects Of The Renal System - Shnyra Flashcards

1
Q

isschemic AKI leads to what

A

Metabolic Acidosis + ATP depletion

Acute renal Failure

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2
Q

Acute renal failure

A

abrupt decrease in kidney function

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3
Q

major cause of AKI

A

sterile inflammation (hypoxia)
when necrosis from ischemia of kidney tissue OR ECM causes DAMP release
= activate APCs, C-Reactive Proteins —-> CP, TLRs

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4
Q

C-reactive proteins activate what

A

classical pathway

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5
Q

wha do APCs release

A

TNF-a, IL-6, IL-1B

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6
Q

when complement pathway is activated on kidney cells what happens

A

C3a and C5a are also chemoattractants = inflammation + death of cell

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7
Q

reason kidney is so susceptible to complement activation

A

high filtration rate causes deposition of immune complexes

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8
Q

profibrotic factors

A

TGF-B = activate fibroblasts

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9
Q

most N and M come to kidney from

A

Complement activation

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10
Q

how are phagocytes activated

A

Fc-receptor

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11
Q

N release what

A

proteases, free radicals

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12
Q

what do monocytes release

A

—-> M1 that go into glomeruli,
NO, ROS, cytokines, GFs, chemokines
= vascular injury and cell proliferation

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13
Q

early AKI

A

Th1, Th17, M1

tissue injury

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14
Q

AKI tissue repair is done by what cells

A

M2

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15
Q

Late AKI

A

Th1

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16
Q

what is the function of Th17 cells steps

A
  1. APC + CD4 cell
  2. Th17 cells activated release IL17, IL22
  3. IL17 bring release CCL20 for inflammation
  4. IL22 controls homeostasis and increased barrier function
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17
Q

what happens what TH17 cells release IL17

A

CCL20 is expressed which activates:

N, M, Th1—-> M1, TH17

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18
Q

what does Th1 cells secrete

A

INF-g to recruit M1 cells + IgG that bind to Fc receptors

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19
Q

what activated Th1 cells

A

APC —-> IL12

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20
Q

what do Th2 cells release

A

IL13, IL4 —-> M2

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21
Q

what do M2 cells release

A

TGF-B, IL10 (pericyte accumulation, myofibroblast differentiation, ECM production)

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22
Q

how are M1 —-> M2

A

M reprogramming (CSF-1 (M-CSF), IL10

23
Q

CD25 causes what cytokine

24
Q

Treg cells and AKI

A

low Tregs leads to increased AKI risk

25
Q

Treg has what receptor important for preventing AKI

26
Q

AKI can be what types of hypersensitivity

27
Q

Type 2 AKI

A

IgG, IgM, cell bound Ag

Complement activation + lysis

28
Q

Type 3 AKI

A

IgG, IgM, soluble Ag
Ab-Ag deposited in tissues
Complement activation and Neutrophils

29
Q

which HLA is most important in transplant testing

A

HLA 1 (since HLA 2 is only on APCs that are mostly killed in the donor organ)

30
Q

H vs G Hyperacute

A

Type 2
Abs, complement : ABO blood type mismatch
immediate

31
Q

H vs G Acute

A

Type 4
T-cells, Th1, Th17, CD8+
Days to weeks

32
Q

H vs G Chronic

A

Type 3,4
due to vascular trauma, T-cells, CD4, M2, Abs (maybe Th1)
Months to years
has to do with quality and timing of transplant

33
Q

autograft
isograft
allograft
xenograft

A

same person
identical twin
same species
different species (can cause rapid complement attack)

34
Q

4 things for a good transplant

A
  1. quality of organ + allograft
  2. HLA matching
  3. host anti-donor response strength should be low
  4. apply immunosuppression
35
Q

when a damaged graft is transplanted what happens in steps

A
  1. graft tissues release DAMPS
  2. Clotting cascade (fibrin) + increase permeability of leukocytes
  3. Kinin cascade : vasodilation + permeability
  4. hyperacute if not controlled
36
Q

ABO matching is not important when and for what reason

A
  1. cornea, heart valve, bone, tendon
    = non-vascularized + limited immune cell access
  2. stem cells (they have no HLA1)
37
Q

ABO incompatibility for kidney transplant can still be done how

A

by intensified immunosuppression

38
Q

Microcytotoxicity Test

A
  1. recipient Abs are added to donor cells
  2. add complement
  3. add dye
  4. if dye is inside cells = Abs attacked donor cells
39
Q

Microcytotoxicity Test for HLA 1

A
  1. get lymphocytes from spleen/ LN (donor) + peripheral blood (recipient)
  2. Anti-HLA (from volunteers) added
  3. add complement and add dye
  4. if both donor lymphocyte and recipient lymphocyte act the same to anti- HLA = MATCH
40
Q

Microcytotoxicity Test for HLA 2

A
  1. T-cells from R and D (Dead after radiation) are added
  2. R T-cells need to find the D Ag-Tcell or Ag-DC and proliferate
  3. the more R t-cells proliferate = the more of a mismatch
41
Q

adaptive allograft rejection is stronger then adaptive pathogen response becuz

A

more t-cells are activated

42
Q

if reaction happened to first graft then second graft from same donor

A

will be even stronger and so extensive testing should be done before

43
Q

Direct allorecognition

A
  1. R T-cells start to come to organ when BF increases
  2. R T-cells find DAMPS —-> D DC
  3. D DC go to LN —-> R T-cells (LN)
44
Q

Indirect Allorecognitino

A
  1. R T-cells start to come to organ when BF increases
  2. R T-cells find DAMPS —-> R DC
  3. R DC go to LN to tell more R T-cells
45
Q

Th2 allograft rejection

A

Th2 —-> IL4, IL5 —-> Abs (humoral)

46
Q

Th1 allograft rejection

A

Th1 —-> IL2, IFN-g —-> CD8+ (cell mediated)

47
Q

Acute H vs G rejection steps

A
  1. D T-cells –> D DCs (from DAMPS)
  2. D DCs —-> LN
  3. activate R T-cells
  4. CD8+ type 4 HS,
    * direct + indirect pathway and TLRs
48
Q

Chronic H vs G rejection happens due to

A

ischemia from occluded BVs (from chronic rejection)

  1. M2 release TGF-B = SM proliferation
  2. Abs —-> complement
    * *** does not respond to immunosuppressents
    * indirect pathway + Abs
49
Q

other things that could cause chrinic rejection

A
  1. ischemic reperfusion before transplant
  2. own kidney failure
  3. nephrotoxicity (Cyclosporine A) = immunosuppressants for preventing acute rejection
50
Q

G vs H

what is the cause

A

Type 4 (usually BM, Liver, GI that you cant kill all donor APCs and t-cells)

  1. Donor T-cells proliferate and attack R minor H-Ags on its T-cells
  2. D T-cells go to LN and make R -Tcells attack its own immune system (HLA 1 and HLA 2)
    - usually in immunosuppressed people
    - CD8+, CD4+
51
Q

G vs H
Sx:
how to Tx:

A

jaundice
D, Rash
Tx : DONT use immunosuppressants

52
Q

Acute G vs H

A

cell death

jaundice , Rash, D, GI hemorrhage

53
Q

Chronic G vs H

A

Fibrosis + atrophy

Dysfunction of organ

54
Q

2 ways G vs H kill target cells

A
  1. Fas-FasL (CD3, TCR)
  2. Perforin/Granzyme (DNA fragments)
    * * BOTH USE CD8+ (CTL)**

CPR Exam 2 (22 decks)

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