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

Immunological Aspects Of The Renal System - Shnyra Flashcards

(54 cards)

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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

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A

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

23
Q

CD25 causes what cytokine

24
Q

Treg cells and AKI

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A

low Tregs leads to increased AKI risk

25
Treg has what receptor important for preventing AKI
ANTI-CD25
26
AKI can be what types of hypersensitivity
2, 3
27
Type 2 AKI
IgG, IgM, cell bound Ag | Complement activation + lysis
28
Type 3 AKI
IgG, IgM, soluble Ag Ab-Ag deposited in tissues Complement activation and Neutrophils
29
which HLA is most important in transplant testing
HLA 1 (since HLA 2 is only on APCs that are mostly killed in the donor organ)
30
H vs G Hyperacute
Type 2 Abs, complement : ABO blood type mismatch immediate
31
H vs G Acute
Type 4 T-cells, Th1, Th17, CD8+ Days to weeks
32
H vs G Chronic
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
autograft isograft allograft xenograft
same person identical twin same species different species (can cause rapid complement attack)
34
4 things for a good transplant
1. quality of organ + allograft 2. HLA matching 3. host anti-donor response strength should be low 4. apply immunosuppression
35
when a damaged graft is transplanted what happens in steps
1. graft tissues release DAMPS 2. Clotting cascade (fibrin) + increase permeability of leukocytes 3. Kinin cascade : vasodilation + permeability 4. hyperacute if not controlled
36
ABO matching is not important when and for what reason
1. cornea, heart valve, bone, tendon = non-vascularized + limited immune cell access 2. stem cells (they have no HLA1)
37
ABO incompatibility for kidney transplant can still be done how
by intensified immunosuppression
38
Microcytotoxicity Test
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
Microcytotoxicity Test for HLA 1
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
Microcytotoxicity Test for HLA 2
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
adaptive allograft rejection is stronger then adaptive pathogen response becuz
more t-cells are activated
42
if reaction happened to first graft then second graft from same donor
will be even stronger and so extensive testing should be done before
43
Direct allorecognition
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
Indirect Allorecognitino
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
Th2 allograft rejection
Th2 ----> IL4, IL5 ----> Abs (humoral)
46
Th1 allograft rejection
Th1 ----> IL2, IFN-g ----> CD8+ (cell mediated)
47
Acute H vs G rejection steps
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
Chronic H vs G rejection happens due to
ischemia from occluded BVs (from chronic rejection) 1. M2 release TGF-B = SM proliferation 1. Abs ----> complement * *** does not respond to immunosuppressents * indirect pathway + Abs
49
other things that could cause chrinic rejection
1. ischemic reperfusion before transplant 2. own kidney failure 3. nephrotoxicity (Cyclosporine A) = immunosuppressants for preventing acute rejection
50
G vs H | what is the cause
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
G vs H Sx: how to Tx:
jaundice D, Rash Tx : DONT use immunosuppressants
52
Acute G vs H
cell death | jaundice , Rash, D, GI hemorrhage
53
Chronic G vs H
Fibrosis + atrophy | Dysfunction of organ
54
2 ways G vs H kill target cells
1. Fas-FasL (CD3, TCR) 2. Perforin/Granzyme (DNA fragments) * *** BOTH USE CD8+ (CTL)****

CPR Exam 2 (22 decks)

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