36. Transplant rejection Flashcards Preview

Immunology > 36. Transplant rejection > Flashcards

Flashcards in 36. Transplant rejection Deck (32):
1

Types and onset (timw)

1. hyperacuteetns> ut
2. acute --> weeks to months
3.chronic --> months to years
4. graft vs host disease --> varies

2

Hyperacute -pathogenesis

pre-existing recipient antibodies react to donor antigen and activate complement (type II hypersensivity reaction)

3

Hyperacute - result/onset

widespead thrombosementi-manags of graft vessels --> ischemia / necrosis onset : within minutes

4

Hyperacute transplant rejection management

graft must be removed

5

acute transplant rejection- mechanism

1. cellular : CD 8 T cells activated against donor MHCs (( type IV hypersensivity reaction)
2. Humoral: antibodies formation (after transplant) --> activate complement

6

acute transplant rejection results in / onset

Vasculitis of graft vessels with dense interstitial lymphocytes infiltrate
onset:weeks to months

7

acute transplant rejection management

prevent/reverse with immunosuppresant

8

chronic transplant rejection-mechanism

CD4 T cells respond to recipient APCs presenting donor peptides, including allogenic MCR --> cytokines --> cellular and homural compoments (type II and IV hypersensivity reactions)

9

chronic transplant rejection - results in / onset

cytokines --> proligeration of vascular SMCs, parencymal, atrophy , intestitial fibrosis
Dominated By ARTERIOSCLEROISIS
onset one month

10

Chronic transplant rejection -lung

bronchiolitis obliterans

11

Heart

accelarated atherosclerosis

12

Kidney

chronic graft nephropathy

13

Liver

vanishing bile duct syndrome

14

Bronchiolitis obliterans

bronchioles are compressed and narrowed by fibrosis ( scar tissue ) and/or inflammation --> life threating form f non-reversible

15

Graft vs host disease - Mechanism/ ons

.

16

GVHD requiremenents to oocur

.

17

GVHD potentially beneficial

leukemia

18

Graft versus tumor effect - definition

Donor T- cells eliminate malignant residual host T-cells (graft versus leukemia) or eliminates diverse kinds of tumors

19

Transplant rejection - types , onset 9time) and hypersensicity reaction

.

20

• Hyperacute rejections occur within ____ (minutes/weeks/years) of transplant, due to activation of antibodies in the ____ (donor/recipient).
Minutes, recipient (graft vessels are occluded, causing ischemia and necrosis)
• What is the pathogenesis of acute graft rejection, and what do you expect to see on histology?
Cytotoxic T cells react against foreign MHCs; you expect vasculitis of graft vessels with dense interstitial lymphocytic infiltrates
• How long after transplantation do patients develop the symptoms of acute transplant rejection? How can acute rejection be reversed?
Acute rejection occurs within weeks to months of transplantation; use of immunosuppressants such as cyclosporine and muromonab-CD3 (OKT3)
• What process mediates chronic transplant rejection. Can it be reversed? How long after transplantation does it tend to manifest?
Antibody-mediated and T-cell–mediated; no, it is irreversible; months to years
• Which members of the immune system are involved in chronic rejection? What findings are seen in the graft vessels and tissues?
Antibodies and T cells are implicated; proliferation of vascular smooth muscle and parenchymal fibrosis/prominent arteriosclerosis
• A transplantation patient with a maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea is likely to have had what transplantation?
Bone marrow or liver (lymphocyte-rich tissue, initiating graft-versus-host disease)—potentially beneficial in bone marrow transplantation
• What is the pathogenesis of graft-versus-host disease, and what do you expect to see histologically?
Grafted immunocompetent T cells in the immunocompromised host reject cells with foreign proteins, causing severe organ dysfunction
• Years after a kidney transplant, a patient develops glomerulopathy. What is the mechanism for this rejection? Is it reversible?
T cells and antibodies react against donor antigens in chronic rejection; irreversible
• A woman has a liver transplant and develops vasculitis within weeks. What are the cellular and humoral responses to her transplant?
Cellular responses = Tc cells react against donor MHC, humoral responses = newly formed antibodies react (type II) and enable complement
• A man is receiving a kidney transplant. Within minutes, the kidney undergoes necrosis. What is pathogenesis of this reaction? Treatment?
Preexisting antibodies attack donor cells (type II reaction) and enable complement; remove graft (this is hyperacute transplant rejection)

.

21

Transplant rejection - types , onset 9time) and hypersensicity reaction

1. Hyperacute- minutes-type 2
2. Acute --> weeks to months --> type 2 (humoral) or IV (cellular)

3. chronic --> months to years --> both IV and IC (humoral cellular)
4. graft vs host disease-->varies-->type IV

22

• Hyperacute rejections occur within ____ (minutes/weeks/years) of transplant, due to activation of antibodies in the ____ (donor/recipient).


Minutes, recipient (graft vessels are occluded, causing ischemia and necrosis)

23

How long after transplantation do patients develop the symptoms of acute transplant rejection? How can acute rejection be reversed?

Acute rejection occurs within weeks to months of transplantation; use of immunosuppressants such as cyclosporine and muromonab-CD3 (OKT3)

24

Which members of the immune system are involved in chronic rejection? What findings are seen in the graft vessels and tissues?

Antibodies and T cells are implicated; proliferation of vascular smooth muscle and parenchymal fibrosis/prominent arteriosclerosis

25

• A transplantation patient with a maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea is likely to have had what transplantation?

Bone marrow or liver (lymphocyte-rich tissue, initiating graft-versus-host disease)—potentially beneficial in bone marrow transplantation

26

What is the pathogenesis of graft-versus-host disease, and what do you expect to see histologically?

Grafted immunocompetent T cells in the immunocompromised host reject cells with foreign proteins, causing severe organ dysfunction

27

Years after a kidney transplant, a patient develops glomerulopathy. What is the mechanism for this rejection? Is it reversible?

T cells and antibodies react against donor antigens in chronic rejection; irreversible

28

A woman has a liver transplant and develops vasculitis within weeks. What are the cellular and humoral responses to her transplant?

Cellular responses = Tc cells react against donor MHC, humoral responses = newly formed antibodies react (type II) and enable complement

29

• A man is receiving a kidney transplant. Within minutes, the kidney undergoes necrosis. What is pathogenesis of this reaction? Treatment?

Preexisting antibodies attack donor cells (type II reaction) and enable complement; remove graft (this is hyperacute transplant rejection)

30

Years after a kidney transplant, a patient develops glomerulopathy. What is the mechanism for this rejection? Is it reversible?

T cells and antibodies react against donor antigens in chronic rejection; irreversible

31

A woman has a liver transplant and develops vasculitis within weeks. What are the cellular and humoral responses to her transplant?

Cellular responses = Tc cells react against donor MHC, humoral responses = newly formed antibodies react (type II) and enable complement

32

A man is receiving a kidney transplant. Within minutes, the kidney undergoes necrosis. What is pathogenesis of this reaction? Treatment?

Preexisting antibodies attack donor cells (type II reaction) and enable complement; remove graft (this is hyperacute transplant rejection)