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CPR > Renal Immunology > Flashcards

Renal Immunology Flashcards

1
Q

What is one of the major causes of Acute renal failure ARF

A

Ischemic acute kidney injury leading to metabolic acidosis and ATP depletion

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2
Q

What induces sterile renal inflammation

A

DAMPs released from dying parenchymal cells or during ECM degradation and remodeling
Activate PRRs causing release of TNFa, IL-6, IL-1

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3
Q

What activates complement pathways and what type of receptors are activated to induce innate immune response in sterile renal inflammation

A 
CRP binds damps activating complement classic pathway
Immune cells (dendritic, macrophage, endothelial cells) recognize DAMPs via TLRs inducing innate immune response
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4
Q

Macrophage activation

A

IFN-y is major cytokine activating macrophages

Macrophages are single largest contributor to inflammatory cytokines in body

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5
Q

M1 vs M2 macrophage

A

M1 play key role in acute kidney injury
-induced by PAMPs and DAMPs binding TLR/PRR
-IFN-y promotes their differentiation
-release IL-1/12/23, ROS/NO
M2 play key role in tissue repair
-activated by IL-4/13
-release IL-10 and TGF-b promoting repair

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6
Q

Early stage vs late stage of AKI what T cells dominate

A

Early stage is Th17 cells

Late stage is Th1 cells

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7
Q

Macrophage reprogramming

A

M1 macrophages can be reprogrammed to M2 macrophages by CSF-1 and IL-10

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8
Q

Macrophage stimulation of matrix deposition/tissue repair

A

Profibrotic factors TGF-b and PDGF attracting pericyte accumulation which differentiate into myofibroblasts and produce ECM

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9
Q

Th17 function

A

Secrete IL-17 stimulating resident renal cells to produce inflammatory mediators
IL-17 induces expression of CCL20 (MIP3-macrophage inflammatory protein 3) leading to neutrophil (mainly), monocyte, Th1 and Th17 cell recruitment

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10
Q

What causes the kidneys unique susceptibility to complement induced damage

A

Filtration favors tissue deposition of immune complexes

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11
Q

Compliment pathway role in damage

A

AKI and tissue damage leads to excessive generation of DAMPs which activate resident immune cells via PRRs
C3b and C5a activation causes further activation of tissue resident cells
Deposition of membrane attack complex leads to massive cell death

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12
Q

Which types of hypersensitivity reactions usually occur in AKIs

A

Type II and Type III

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13
Q

Type II hypersensitivity

A

IgG or IgM mediated
Formed by cell-bound antigen
IgG/IgM Ab binds to cellular antigen, leading to complement activation and cell lysis
Ex. Anti-glomerular basement membrane (GBM) antibody-mediated glomerulonephritis (Positively charged Ags are planted on the negatively charged GBM, leading to type II hypersensitivity reaction)

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14
Q

Type III hypersensitivity

A

IgG or IgM mediated
Formed by soluble antibody
Antigen-antibody complexes are deposited in tissues
Complement activation provides inflammatory mediators and recruits neutrophils
Enzymes released from neutrophils damage tissues
Ex. Post streptococcal glomerulonephritis, rheumatoid arthritis, SLE

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15
Q

Xenografts

A

Exchanged b/w members of different species
Very susceptible to rapid attack by naturally occurring Abs activating complement
Insertion of human genes into genome of donor animal can help

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16
Q

What molecules are released by graft tissues leading to host immune responses and possible hyperacute allograft rejection

A

Mechanical trauma and ischemia-reperfusion injury (AKI) to graft tissues causes release of DAMPs, triggering the clotting cascade, which leads to increased vascular permeability and neutrophil/monocyte attraction
Also leads to kinin cascade w/bradykinin, causing vasodilation, smooth muscle contraction and further increasing vascular permeability
If these early responses aren’t controlled, you end up with hyperacute allograft rejection

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17
Q

ABO incompatible kidney transplant

A

Used to be absolute contraindication due to risk of hyperacute rejection
Now with better immunosuppression, ABOi-KT outcome is comparable to ABO compatible

18
Q

ABO matching is not important for what types of transplantations

A

Corneal transplant, heart valve transplant, bone and tendon grafts (nonvascularized tissues)
ABO incompatibility is not a contraindication to stem cell transplantation

19
Q

What Ig reacts with blood type antigens

A

Most likely IgM because they are carbohydrate antigens

20
Q

Microcytotoxicity test for pre-existing non-ABO Abs against donor

A

Recipient serum with Abs is added to donor cells
Complement is added
Dye is added
If dye accumulates in the cells, that means a MAC complex was formed and there are indeed preformed Abs present

21
Q

The success of transplantation is dependent on matching of

A

HLA Ags

22
Q

What HLA class is strongest barrier to transplantation

A

HLA class I because all nucleated cells express them

23
Q

Mixed lymphocyte response

A

Donor cells are radiated so they cannot proliferate but can serve as APCs
Mixed with recipient cells and lymphocytes + H-thymidine
If recipient cells proliferate and radioactive thymidine is seen- HLA class II of recipient does not match donor cells
If no radiation seen/no proliferation - good for transplant

24
Q

Sequence of events in allograft rejection

A

APCs trigger CD4/CD8 T cells
Both a local and systemic immune response develop
Cytokines recruit and activate immune cells
Development of specific T cells, NK cells, or macrophage mediated cytotoxicity
Allograft rejection

25
Q

Host vs graft disease

A

When a kidney is transplanted and the recipients T cells attack the transplant
Adaptive immune response
If a second graft is performed from the same donor, it is rejected more rapidly

26
Q

Direct allorecognition

A

T cells recognize intact allogenic MHC molecules on the surface of donor antigen-present cells in the graft

27
Q

Indirect allorecognition

A

Alloantigens are recognized in the context of recipients MHC class II molecules after they have been processed and presented by recipient APCs

28
Q

Host vs graft response trigger

A

Non-immune injury of the graft (DAMPs released) activates endothelial cells, and T cells enter the allograft
Ag specific T cells interact with APC and become stimulated, release cytokines which further the process

29
Q

Effector mechanisms of host vs graft response

A

Humeral rejection - Th2 - IL-4, 5, 10

Cellular rejection - Th1 - IL-2, IFN-y

30
Q

Hyperacute rejection

A

Occurs immediately
Type II hypersensitivity - Humeral response caused by accidental ABO blood type incompatibility or previous sensitization to Ags- Preformed Ab mediated complement activation, endothelial damage, inflammation and thrombosis

31
Q

Acute rejection

A

Occurs in weeks to months
Type IV hypersensitivity - Cell mediated response against foreign MHC- can be both CD4/CD8 mediated
Donor DCs (passenger leukocytes) play important role in triggering rejection
Donor DCs migrate to lymph nodes and stimulate a primary immune response in recipient lymphocytes
There can also be some indirect response involved
Most common type

32
Q

Chronic rejection

A

Occurs in months to years
Type IV hypersensitivity - Cell mediated response (mainly an indirect response) resulting from foreign MHC “looking like” a self MHC carrying an antigen - M2 macrophages and T cells
Deposition of complement/Ab complexes can also be involved
Chronic DTH reaction in vessel wall, intimal smooth muscle proliferation (repair process), vessel occlusion and ischemia

33
Q

Important non-immunologic factors in chronic rejection

A

Ischemia-reperfusion damage
Recurrence of the disease that caused failure of kidney
Nephrotoxicity of drugs
-Chronic rejection does not respond to immunosuppressive therapy

34
Q

Graft vs host disease

A

Reaction of grafted mature T cells in bone marrow is directed against Minor H Ags of the recipient when HLA Ags are usually matched
Occurs in the immunocompromised recipients because their immune system is unable to reject the allogeneic cells in the graft

35
Q

Acute GVHD

A

Epithelial death in the skin, liver and GI

-Rash, jaundice, diarrhea

36
Q

Chronic GVHD

A

Fibrosis and atrophy of the affected organ

  • may lead to complete dysfunction of the affected organ
  • may produce obliteration of small airways
37
Q

What tissues are commonly involved in GVHD

A

Small bowel, lung, liver- they naturally contain a number of T cells

38
Q

GVHD mechanisms

A

Donor APC recognize recipient Ag and activate donor CD4/CD8 cells by cross presentation
Cell killing mediated by Fas-FasL or Perforin/Granzyme methods

39
Q

Examples of DAMPs and what receptor recognizes them and what downstream pathway they activate

A

HMGB1- RAGE
Uric Acid- NLRP3
HSPs- Scavenger receptor class A
All activate NF-kB pathway

40
Q

Activated T cells release what cytokines to activate Th1, Th2 and Th17 cells, respectively

A

Th1- IL-12 –> antigen presentation/cellular immunity
Th2- IL-4 –> humoral immunity and allergy
Th17- IL-6/TGF-B –> tissue inflammation

CPR (24 decks)

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