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CPR Final Exam > Renal Immunology > Flashcards

Renal Immunology Flashcards

1
Q

Ischemic Acute kidney injury leads to what kind of acidosis?

A

metabolic acidosis

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2
Q

AKI causes ___.

A

Acute renal failure

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3
Q

What induces sterile renal inflammation?

A

Intrinsic DAMPs released by necrotic parenchymal kidney cells due to the ECM degradation

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4
Q

What is another name for DAMPs?

A

alarmins

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5
Q

What do alarmins represent?

A

Intracellular molecular structures such as HMGB1, Uric acid, HSP’s, S100 protein, Hyaluronans

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6
Q

What recognizes DAMPs?

A

TLR expressed on immune cells and they become activated and produce renal inflammation

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7
Q

What complement activation pathways have been linked to AKI?

A

All three paths

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8
Q

Why are kidneys uniquely susceptible to complement induced damage?

A
  • Because the high filtration rate favors tissue deposition of immune complexes
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9
Q

What drives infiltration of neutrophils and monocytes in AKI?

A

C5a an C3a

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10
Q

What do neutrophils release in an AKI?

A
  • Proteases which cause degradation of GBM
  • Oxygen derived free radicals which cause cell damage
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11
Q

Monocytes differentiate into what type of macrophage and what do they release and infiltrate?

A
  • Differneitate into M1 and infiltrate the glomeruli
  • Release:
    • ROS
    • Cytokines/Chemokines
    • Growth factors
    • Eicosanoids
    • NO
  • All of these contribute to vascular injury and cell proliferation
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12
Q

In the early stage of AKI what mediates immune responses?

A
  • Th17 and Th1 cells dominate in causing tissue injury
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13
Q

What macrophages are involved in AKI?

A
  • M1 plays a key role in AKi
  • M2 play a key role in tissue repair
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14
Q

In the late stage of AKI, what cell type dominates?

A

Th1

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15
Q

What induces Th17?

A
  • IL1 IL6 and TGF-B prodducedby DC’s
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16
Q

Compare IL17 vs IL22

A
  • 17 contributes to inflammation when its in greater ammounts than IL22
  • IL22 controls homeostatsis when greater than IL 17
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17
Q

IL-17 indudces expression of CCL20 which leads to recruitement of what cells?

A
  • Neutrophils
  • Monocytes
  • Th1 and Th17 cells

This recruitement leads to progression of immune mediated kidney damage

  • Th1 secretes IFN-y inducing M1
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18
Q

Treg role in AKI?

A
  • Prevent AKI progression and restrict inflammation and promote repair and regeneration
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19
Q

What is host vs graft disesase and the three categories?

A
  • Caused by rejection of transplant by host’s immune system
    • hyperacute rejection immediate and caused by an Ab
    • acute rejection occurs days to weeks after and caused by T cells
    • Chronic rejection seen months or years after transplant and is caused by vascular trauma, inflammatory products of T cells and Ab’s
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20
Q

What is graft vs host disease and the types?

A
  • Reactions of donor immune cells to the host and it can be chronic or acute
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21
Q

Autograft?

A
  • graft from the same person, move from one part of body to another
    • skin graft, coronary bypass
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22
Q

Isograft?

A
  • Graft between identical twins
23
Q

Allografts?

A
  • Graft betweeen nonidentical members of same species
24
Q

Xenograft? Cons? How is it done?

A
  • grafts exchanged btw species
  • succeptible to rapid attack caused by Abs that will activate complement
  • Human HLA genes are inserted into genes of donor animals and increase the chance of successful transplant
25
Q

What is the outcome of a transplant determined by?

A
  • Condition of allograft
  • Donor host antigenic disparity
  • Strength of anti donor response
  • Applied immunosuppression
26
Q

How does mechanical trauma and IRI impact the outcome of fa kidney transplant?

A
  • A damaged graft will release DAMPs triggering
    • clotting casacade generating fibrin
    • fibrin aggregates to form clot
    • fibrinopeptides increase vascular permeability and leukocyte accumulation
    • kinin cascade produces bradykinin that cause vasodilatioin and sm mm contraction and increases vascular permeabiltiy
  • Results in hyperacute rejection
27
Q

What areas in the body are ABO matching not important?

A
  • Cornea
  • Heart valve
  • Bone
  • Tendon

  • Tissues aren’t vascularized and have limited access for immune cells*
  • ABO incompatibility also doesn’t impact stem cell transplant*
28
Q

What Ab’s are present on Type A blood cells?

29
Q

What Abs are on group O?

A

Anti A and Anti B

30
Q

What Ab’s are on those with AB blood?

31
Q

How do you do blood typing?

A
  • RBC’s + anti A or Anti B + complement system
  • Celll lysis by MAC occurs
32
Q

What is the microcytotoxicity test for preformed Abs?

A
  • Recipient serum with Abs is added to the donors cells
  • Add complement proteins and a dye that does NOT accumulate inside cells
  • If the recipient has Ab’s for the donor classic complement path occurs and MAC forms
    • Pores in the cell will allow the dye to accumulate inside the cell
  • Mismatch because preexisting Abs are foun in the recipient
33
Q

Microcytotoxicity for Class I HLA compatiblity?

A
  • Take HLA-A3 Ag, donor cell WBC, and recipient WBC and add together
  • Complement is added and classical activation occurs if a complex was formed
  • Dye is aded
  • If accumulated in both donor and recipient cells it means HLA-A3 is found in both and they match
  • Test HLA-A7 repeat process to see if more match

Need multiple HLA matches not just one

34
Q

Mixed lymphocyte response for Class II HLA?

A
  • Isolate donor T cells and expose to radiation so they can’t proliferate, but can still sesrve as APC’s
  • Add recipient T cell labelled thymidine
  • If recipient T cell finds Ags on donor DC they will be activated and proliferate
  • During cell division DAN is replicated and thymidine is incorporated into DNA
    • more radioactivity=greater class II disparity btw donor and recipient
  • replicated DNA with thymidine means donor and recipient don’t have class II compatiblity
35
Q

What immune responses are seen with HVGD?

A
  • CD4 CD8 respond against graft Ags
  • systemic and local responses develop
  • cytokines recruite and activate immmune cells
  • Cytotocix reactions mediated by CD8 and NK cells and macrophages occurs
  • allograft rejectionn occurs
36
Q

What type of immunity mediates graft rejection?

A

Innate and adaptive

37
Q

Why are adaptive immune responses against a graft much mroe vigorous and strong than response against a virus?

A
  • High frequency of T cells that recognize that graft as non cells
    • un immunized individual has <1/100,000 T cells that will respond with exposure to virus
    • About 1:100 to 1:1,000 T cells respond to allogenic Ags
38
Q

What is direct allorecognitioni?

A
  • Recipient T cells arrive into the graft and recognize the MHC molecules on the donors APC’s in the graft
39
Q

What is indirect allorecognition?

A
  • Donor MHC molecules are taken up and processed and presented by the recipient APC’s for activation of the recipients T cells
40
Q

In HVGD what do activated T cells release?

A
  • IFN-y and TNF which will activate APCs further and endothelial cells and increase # leukocytes present
41
Q

Effector mechanisms of graft rejection are from what cell and cytokines?

A
  • Th2 releasing IL-4 and IL-5 humoral rejection mediated by ABs
  • Th1 releasing IL-2 and iFN-y cell mediated rejection by CD8 t cells
42
Q

What type of hypersensitivity mediates hyperacute HVGD?

43
Q

What type of hypersensitivity mediates acute and chronic HVGD?

A
  • Acute: IV
  • Chronic: III and IV
44
Q

What type of hypersensitivity mediates graft vs host disease?

45
Q

Mechanism of hyperacute rejection?

A

PReexisting abs and complemment

46
Q

Acute rejection mechanism?

A

Primary activation of TH1 ccells and CTL’s

47
Q

What is mechanism of chronic rejection?

A
  • M2 macrophages and t cells
48
Q

Why may a recipient have pre existing Abs?

A
  • ABO incompatiblity
  • sensitized to donor MHC by previous transplants
  • blood transfusions
  • pregnancy
49
Q

What non immulological factors are important in chronic graft rejection?

A
  • Ischemia reperfusion damage
  • Failure of patient’s own kidney
  • Nephrotoxicity from the drugs used for immunosuppression

chronic rejection doesn’t respond to immunosuppressive therapy

50
Q

leading the response for chronic graft rejection are __ and __.

A
  • CD4 and Macrophages
51
Q

In graft vs host disease what antigens are the response generated towards?

A
  • Minor H Ags bc HLA Ags are usually matched
52
Q

What happens in acute GVHD?

A
  • mediated by epithelial cell death in the skin liver and GI
  • Rash, jaundice, diarrhea and GI hemorrhage
53
Q

What happens in chronic GVHD?

A
  • Mediated by fibrosis and atrophy of the affected organs
  • may lead to complete dysfunction of the affected organ
54
Q

How does GVHD occur?

A
  • The donor APC’s will ltake up and present the recipients Ags in Class I and II MHC
  • This causes activation of donor CD4 and 8 t cells

CPR Final Exam (16 decks)

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