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Year 1 CPR I. Exam 2 > 8. Immunological Aspects of the Renal System > Flashcards

8. Immunological Aspects of the Renal System Flashcards

1
Q

What is the presentation and type of hypersensitivity for graft-versus-host disease?

A

Patients present with diarrhea, rash, and jaundice.

This is a type IV hypersensitivity.

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2
Q

What is the role of Th-17 cells in acute renal injury?

A

Secretes interleukin 17 to begin the pro-inflammatory process, and primarily leads the recruitment of neutrophils.

May also recruit monocytes, Th1, and Th-17 cells, via Macrophage Inflammatory Protein-3 (CCL20)

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3
Q

What are the two effector mechanisms of graft rejection, and what cells mediate them?

A

Humoral rejection – Th2

(activated by IL-4; secretes IL4,5,13)

Cellular rejection – Th1

(activated by IL12, secretes IFN Gamma)

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4
Q

What is an autograft, isograft, allograft, and xenograft?

A

Autograft: between the same individual.

Isograft: between two individuals of identical genetic constructions (identical twins)

Allograft: graft exchange between nonidentical members of the same species

Xenograft: graft exchange between members of different species

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5
Q

What are the time frames for hyperacute, acute, and chronic rejections?

A

Hyperacute: immediate

Acute: days/weeks/months

Chronic: months to years

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6
Q

How does the complement system result in death of renal cells in acute kidney injury? (Three mechanisms.)

A

Directly, via MAC complex, lysing cells.

By releasing C3a and C5a, which stimulate proinflammatory responses in neutrophils and macrophages, which can have two different outcoes:

1) Respiratory burst
2) Alternatively, the same neutrophils can release pro-inflammatory cytokines that cause necrosis of renal cells.

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7
Q

Why might ABO antigens be a barrier to transplantation in someone with O- blood?

A

Because A/B antigens can be present on the organs of individuals without A/B antigens on their red blood cells.

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8
Q

What are the five immune events in allograft rejection?

A

Antigen presenting cells trigger CD4+ and CD8+ T cells

Both a local and systemic immune response develops

Cytokines recruit and activate immune cells

Development of T cell, NK cell, and Macrophage mediated cytotoxicity

Allograft rejection

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9
Q

What is the difference between direct and indirect allorecognition?

A

DONOR-RECIPIENT: During direct allorecognition, T cells recognize intact allogeneic molecules on the surface of donor antigen presenting cells in the graft.

RECIPEIENT-RECIPIENT: During indirect allorecognition, the alloantigens are recognized in the context of the recipient’s own antigen presenting cells – after processing and loading onto MHC class II.

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10
Q

What are the two effector mechanisms of graft-versus-host disease?

A

Fas-FasL

Perforin/Granzyme

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11
Q

Between HLA class-I and class-II, which is the main barrier to transplantation?

A

HLA class I, because it is present on every cell.

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12
Q

What two cytokines induce differentiation into Th17?

A

IL-6 and TGF-beta

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13
Q

What is the mechanism of cytotoxicity in acute graft rejection?

A

The DONOR’s dendritic cells migrate to the host’s lymph nodes, stimulating a response. Once activated, the host’s T cells migrate to the organ – where they generate cytotoxic T cells and induce type IV hypersensitivity reactions.

OR

An indirect response to the donor’s MHC (processing and presentation by host’s MHC II)

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14
Q

How is the mixed lymphocyte response test performed, and what does it test for?

A

Mixed Lymphocyte Response (MLR) tests for Type II compatibilty. The donor cells are irradiated so as not to proliferate, and then are exposed to CD4+ recipient cells. H3-thymidine is added to the broth and is uptaken by the recipient’s cells. If the recipient’s cells respond to the class II MHC of the donor, they will proliferate. Excess H3-thymidine is then washed out of solution, and the H3-thymidine in the cells is counted. If the recipient’s cells responded to the class II HLA of the donor, we will see a large amounts of H3-thymidine remaining –> NOT A MATCH.

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15
Q

What are the five DAMPs discussed in this lecture?

A

HMGB1

Uric acid

HSPs (Heat Shock Proteins)

S100 protein

Hyaluronans in the ECM

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16
Q

How does the complement system cause fibrotic repair in acute kidney injury?

A

C3a and C5a summon neutrophils, which release pro-inflammatory cytokines, which summon M2 macrophages,

17
Q

What are the four variables that determine transplant outcome?

A

The condition of the allograft

Donor-host antigenic disparity

Strength of host anti-donor response

Immunosuppressive regimen

18
Q

What sort of graft can cause graft-versus-host disease?

A

A graft with a significant amount of donor T cells – such as:

Bone marrow

Small bowel

Lung

Liver

19
Q

What is the criteria for chronic kidney disease?

A

A GFR of less than 60 mL/min per 1.73 m² for more than three months.

OR

Signs of kidney damage for greater than three months.

20
Q

How is the micro-cytotoxicity test for preformed antibodies performed?

A

Add the donor’s cells to the recipient’s serum.

Add complement and a special dye.

Examine the donor’s cells under a microscope, to see if the dye entered the cells via the MAC-attack complex.

21
Q

What can be caused by ischemic acute kidney injury?

A

Metabolic acidosis and ATP depletion – leading to acute renal failure

22
Q

How might acute kidney injury trigger autoimmunity?

Which type of hypersensitivity would this be?

A

When the kidneys are injured, positively charged antibodies can interact with the negative glomerular basement membrane. This results in anti-glomerular basement membrane antibody-mediated glomerulonephritis.

This is a type II hypersensitivity.

23
Q

What two things will occur immediately following kidney implantation if the organ is damaged prior to the surgery?

A

The clotting cascade will cause the creation of fibrinopeptides, which will increase vascular permeability, attract neutrophils, and attract macrophages.

The kinin cascade will produce bradykinin, which will increase vascular permeability, cause vasodilation, and smooth muscle contraction.

(Both of these responses together will result in hyper-acute allograft rejection)

24
Q

In renal tissue injury, which T cells predominate in the earlier stages, and which predominate in the later stages?

A

Th-17 cells predominate in the early stages of renal tissue injury.

Th-1 cells predominate in the later stages of renal tissue injury.

25
Q

What are the two functions of M2 macrophages?

What cytokines control these effects?

A

M2 macrophages perform anti-inflammatory effects, and contribute to renal fibrosis.

IL-10 controls anti-inflammatory effects.

TGF-beta is a growth factor for fibroblasts.

26
Q

What induces M1 macrophage action?

A

The binding of PAMPs and DAMPs to Toll-like receptors

27
Q

Which tissues can be transplanted without testing for anti-HLA antibodies?

A

Cornea

Heart valves

Bone

(nonvascularized tissues, minus stem cells)

28
Q

What is the main cytotoxic mechanism in chronic graft rejection?

A

The indirect pathway for allogeneic recognition, followed by type IV hypersensitivity.

29
Q

What promotes differentiation of macrophages in acute kidney injury?

A

Interferon gamma and other pro-inflammatory cytokines

30
Q

What is the function of macrophage inflammatory protein-3?

(a.k.a. MIP-3, a.k.a. CCL20)

A

Secreted by Th-17 cells to recruit monocytes, Th1 cells, and other Th-17 cells.

31
Q

What interleukins induce differentiation of M2 macrophages?

A

IL-4 and IL-13 produced by T cells

32
Q

Why can an injury to a graft cause a host-versus-graft response?

A

Because the DAMPs activate endothelial cells and cause T cells to enter the allograft.

Once they do, they interact with donor APC and become stimulated – ultimately causing cytotoxicity.

33
Q

For what for transplant types is ABO matching nonessential?

A

Corneal transplant

Heart valve transplant

Bone and tendon transplant

Stem cell transplant

34
Q

What is the criteria for acute kidney injury?

A

A 50% increase in serum creatinine levels within seven days.

OR

An increase in serum creatinine by .3 mg/dL within two days.

OR

Oliguria

35
Q

What type of hypersensitivity do we see in hyperacute, acute, and chronic rejections?

A

Hyperacute is type II hypersensitivity

Acute and chronic are type IV hypersensitivities

36
Q

Why is the immune response against an incompatible graft so much more significant than the response to a pathogen?

A

Because up to 100 times more T cells can respond to an allergenic (donor) APC than to a microscopic pathogen.

37
Q

What is the mechanism for cytotoxicity in hyperacute graft rejection?

A

Pre-existing antibodies cause complement activation via the classical pathway – which leads to death of the endothelium

Year 1 CPR I. Exam 2 (33 decks)

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