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Renal-1 > Immune Aspects of the Renal System > Flashcards

Immune Aspects of the Renal System Flashcards

1
Q

What is an acute rejection caused by?

A

Primary activation of T cells (Th1 cells and CTLs) –> parenchymal cell damage, interstitial inflammation

donor DCs migrate to lNs –> generate response

weeks to months

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2
Q

What compliment pathways have been linked with kidney diseases?

A

all of them!

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3
Q

What cascade occurs when graft tissues are damaged?

A

clotting cascade –> fibrin and fibrinopeptides –> fibrinopeptides = vascular permeability and attract neutrophils and macrophages –> bradykinin –> vasodilation, sm m contraction, etc

if uncontrolled –> hyperacute rejection

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4
Q

What T cells predominate in earlier stages of renal tissue injury?

What about late stages?

A

Th17 = early

Th1 = late

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5
Q

What are convenient sources of lymphocytes for HLA typing?

A

spleen and LN (from cadavers)

peripheral blood

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6
Q

How can some transplant recipients have pre-existing Abs to a graft?

A

ABO blood group incompatibility

recipient has been sensitized to donor MHC by previous transplants, multiple blood infusions, or pregnancy

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7
Q

How do you do specific microcytotoxicity test for class I HLA?

A

Have separate containers w/ donor cells and recipient cells

add Abs –> add complement –> add dye –> If both donor and recipient cells accumulate dye = have identical HLA Ags

If only one type of cell accumulates dye –> Ags are different!

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8
Q

What are the immune events in allograft rejection?

A
  1. APCs trigger CD4 and CD8 T cells
  2. botha local and systemic immune response develop
  3. cytokines recruit and activate immune cells
  4. development of specific T cells, NK cells, or macrophage-mediated cytotoxicity
  5. Allograft rejection
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9
Q

What do Tregs do in AKI?

A

release TGF-beta and IL-10 –> anti-inflammatory

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10
Q

What is C-reactive protein?

A

5 subunit protein (like IgM) –> can activate classical path of compliment

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11
Q

What is type III hypersensitivity and when do you see it in kidney disease?

A

IgG or IgM binds a soluble antigen –> Ag-Ab complexes deposite in tissues –> complement –> neutrophils release enzymes that damage tissue

post-streptococcal GN, rheumatoid arthritis, lupus

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12
Q

What 4 factors determine transplant outcomes?

A
  1. condition of allograft
  2. donor-host antigenic disparity
  3. strength of host anti-donor response
  4. Immunosuppressive regimen
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13
Q

What type of T cell is involved in humoral rejection?

cellular rejection?

A

humoral = Th2

cellular = Th1

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14
Q

What is a xenograft?

A

graft exchanged btw members of different species

particularly susceptible to rapid attack

insertion of human genes into genomes of donor animals increases chances of successful survival

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15
Q

What is the typical source for HLA antisera for specific ags?

A

multiparous women or from planned immunization of volunteers

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16
Q

What is type II hypersensitivity?

A

mediated by IgM or IgG

cell-bound antigen –> Ig binds –> complement activation

see in anti-glomerular basement membrane antibody-mediated GN

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17
Q

What is graft-versus-host disease caused by?

A

reaction of grafted mature T cells with allo-Ags of the host

against minor H Ags

usually for bone marrow transplants, also small bowel, lung, or liver (also contain some T cells)

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18
Q

What is indirect allorecognition?

A

professional APC takes and processes allogeneic MHC molecule –> presents to T cell –> response

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19
Q

How is microcytotoxicity for preformed Abs performed?

A

recipient serum is added to donor cells –> complement added –> dye added

if dye accumulates in cells = preformed Abs for donor cells are present in recipient

This is for HLA I/II Abs

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20
Q

What are the 2 effector mechanisms of GVHD?

A

Fas-FasL

perforin/granzyme

21
Q

What do you see in acute GVHD?

What about chronic?

A

acute = epithelial cell death in the skin, liver, and GI

chronic: fibrosis and atrophy of affected organ

22
Q

What is the function of M2 macrophages in kidney disease?

A

tissue repair and fibrosis

23
Q

What is an allograft?

A

grafts exchanged between nonidentical members of the same species (most transplants)

24
Q

Where are HLA genes located?

A

chromosome

Class I = ABC

Class II = DP, DQ, DR

25
Q

What type of hypersensitivity is GVHD?

A

type 4

26
Q

What is an isograft?

A

graft exchanged btw different individuals of identical genetic makeup (identical twins)

27
Q

Does chronic graft rejection respond to immunosuppressive therapy?

A

no

28
Q

Why is a host vs graft response way higher than against a pathogen?

A

about 1/100 to 1/1000 T cells respond to allogeneic APCs

vs

1/100000 T cells respond to a virus

29
Q

What can stimulate host vs graft response?

A

non-immune injury of the graft (DAMPs) –> activates endothelial cells –> T cells enter allograft

30
Q

What type of hypersensitivity is an acute rxn?

A

IV

31
Q

What is direct allorecognition?

A

T cell directly recognizes unprocessed allogeneic MHC molecule on graft APC

32
Q

Which type of HLA Ag is most important?

A

class I

bc on all cells!

(class II is only on professional APCs)

33
Q

What types of transplants is ABO matching not important for?

A

corneal

heart valve

bone and tendon

= non-vascularized tissues

(also stem cell, but not the same)

34
Q

How are HLA Ags expressed?

A

co-dominantly

35
Q

What type of hypersensitivity is a chronic rejection?

A

type IV

36
Q

What is the hyperacute rejection caused by?

A

preexisting Abs + complement –> endothelial damage, inflammation and thrombosis

immediate

37
Q

What signals induce M2 macrophages?

A

IL-13

IL-14

38
Q

What is chronic rejection caused by?

A

M2 macrophages and T cells –> chronic DTH reaction in vessel wall, smooth muscle proliferation, vessel occlusion

39
Q

What is an autograft?

A

graft exchanged from one part to another part of the same individual

40
Q

What type of hypersensitivity is a hyperacute reaction?

A

type II

41
Q

What is a major factor contributing to GVHD?

A

immunocompromised recipient = can’t reject the allogenic cells in the graft

42
Q

In host vs graft responses, what are the targets for rejection?

A

Histocompatability Ags

43
Q

What signals do M2 macrophages release?

A

IL-10, TGF-beta

44
Q

What signals induce M1 macrophages?

A

TLR-microbial ligands

IFN-gamma

45
Q

What is the significance of mothers in transplantation?

A

mothers much more likely to have antibodies to HLA antibodies bc they will react to baby’s during pregnancy

46
Q

What is the function of M1 Macrophages in kidney disease?

A

acute injuries

direct tubular injury

47
Q

What signals to M1 macrophages release to promote inflamation and phagocytosis?

A

IL-1, IL-12, IL-23 = inflammation

ROS, NO, lysosomal enzymes = phagocytosis

48
Q

How do you do specific testing for class II HLA compatibility?

A

treat donor cells w/ radiation –> mix w/ recipient cells –> add radioactive thymidine –> proliferation of recipient cells occurs

if you see a lot of radioactivity = recipient cells doesn’t share class II MHC of donor

The least radioactivity = best match

49
Q

what important signal does Th17 release to promote inflammation in the kidney? What in turn happens?

A

IL-17 –> stimulates renal cells to produce chemokines and other inflammatory mediators –> primarily recruitment of neutrophils

can also induce CCL20 –> monocytes, Th1, Th17 cells

Renal-1 (14 decks)

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